Min Wang, Xiao-dong Zhang, Han-qing Yang, Yang Li, Wen-mei Chen, An-an Yin
Aim
We aimed to explore the impact of DNA methylation alterations on the DNA damage response (DDR) in melanoma prognosis and immunity.
Material & methods
Different melanoma cohorts with molecular and clinical data were included.
Results
Hierarchical clustering utilizing different combinations of DDR-relevant CpGs yielded distinct melanoma subtypes, which were characteristic of different prognoses, transcriptional function profiles of DDR, and immunity and immunotherapy responses but were associated with similar tumor mutation burdens. We then constructed and validated a clinically applicable 4-CpG risk-score signature for predicting survival and immunotherapy response.
Conclusion
Our study describes the close interrelationship among DNA methylation, DDR machinery, local tumor immune status, melanoma prognosis, and immunotherapy response.
{"title":"DNA methylation variations of DNA damage response correlate survival and local immune status in melanomas","authors":"Min Wang, Xiao-dong Zhang, Han-qing Yang, Yang Li, Wen-mei Chen, An-an Yin","doi":"10.1002/iid3.1331","DOIUrl":"https://doi.org/10.1002/iid3.1331","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>We aimed to explore the impact of DNA methylation alterations on the DNA damage response (DDR) in melanoma prognosis and immunity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Material & methods</h3>\u0000 \u0000 <p>Different melanoma cohorts with molecular and clinical data were included.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Hierarchical clustering utilizing different combinations of DDR-relevant CpGs yielded distinct melanoma subtypes, which were characteristic of different prognoses, transcriptional function profiles of DDR, and immunity and immunotherapy responses but were associated with similar tumor mutation burdens. We then constructed and validated a clinically applicable 4-CpG risk-score signature for predicting survival and immunotherapy response.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our study describes the close interrelationship among DNA methylation, DDR machinery, local tumor immune status, melanoma prognosis, and immunotherapy response.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.1331","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142165631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Qiang Guo, Xin-Yuan Wang, Yan-Chang Zhai, Yong-Wei Dong, Qing-Si He
Introduction
The purpose of this research was to determine how the P53/microRNA-34a (miR-34a)/survivin pathway contributes to oxaliplatin-induced (L-OHP) cell inhibition in gastric cancer.
Methods
The BGC-823 gastric cancer cells were selected, and we examined their viability following treatment with L-OHP at different concentrations and time periods. The expression levels of miR-34a, P53, and survivin in the cells were determined.
Results
In the 12- and 24-h groups, drug concentration of 15 μg/cm² (p < .005 in both) significantly lowered cell viability. In comparison to the control group, miR-34a mRNA expression, P53 mRNA expression, and protein expression were all significantly greater in the 24-h group (p = .0324, p = .0069, p = .0260, respectively), but survivin mRNA and protein expressions were significantly lower than those in the control group (p = .0338, p = .0032, respectively). There was a significant decrease in gastric cancer cells in the miR-34a overexpression group (p = .0020), a significant increase in P53 mRNA and protein expression compared to the control group (p = .0080, p = .0121, respectively), and a significant decrease in survivin mRNA and protein expression compared to the control group. (p = .0213, p = .0069, respectively).
Conclusion
Oxaliplatin inhibits tumor growth, invasion, and metastasis by upregulating miR-34a, activating the expression of the upstream P53 gene, and driving the downregulation of survivin (P53/miR-34a/survivin axis) in BGC-823 gastric cancer cells.
引言 本研究旨在确定 P53/microRNA-34a（miR-34a）/survivin 通路如何促进奥沙利铂诱导的（L-OHP）胃癌细胞抑制作用。 方法 选取 BGC-823 胃癌细胞，检测其在不同浓度和时间段的 L-OHP 处理后的存活率。测定细胞中 miR-34a、P53 和存活素的表达水平。 结果 在 12 小时组和 24 小时组中，药物浓度为 15 μg/cm²（两组的 p 均为 0.005）会显著降低细胞活力。与对照组相比，24 小时组的 miR-34a mRNA 表达量、P53 mRNA 表达量和蛋白表达量均明显增加（分别为 p = .0324、p = .0069、p = .0260），但存活素 mRNA 和蛋白表达量明显低于对照组（分别为 p = .0338 和 p = .0032）。与对照组相比，miR-34a 过表达组的胃癌细胞明显减少（p = .0020），P53 mRNA 和蛋白表达明显增加（分别为 p = .0080 和 p = .0121），survivin mRNA 和蛋白表达明显减少。(分别为 p = .0213 和 p = .0069）。 结论 奥沙利铂通过上调 miR-34a、激活上游 P53 基因的表达和驱动 BGC-823 胃癌细胞中 survivin 的下调（P53/miR-34a/survivin 轴）来抑制肿瘤的生长、侵袭和转移。
{"title":"Oxaliplatin activates P53/miR-34a/survivin axis in inhibiting the progression of gastric cancer cells","authors":"Qiang Guo, Xin-Yuan Wang, Yan-Chang Zhai, Yong-Wei Dong, Qing-Si He","doi":"10.1002/iid3.70004","DOIUrl":"https://doi.org/10.1002/iid3.70004","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>The purpose of this research was to determine how the P53/microRNA-34a (miR-34a)/survivin pathway contributes to oxaliplatin-induced (L-OHP) cell inhibition in gastric cancer.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The BGC-823 gastric cancer cells were selected, and we examined their viability following treatment with L-OHP at different concentrations and time periods. The expression levels of miR-34a, P53, and survivin in the cells were determined.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In the 12- and 24-h groups, drug concentration of 15 μg/cm² (<i>p</i> < .005 in both) significantly lowered cell viability. In comparison to the control group, miR-34a mRNA expression, P53 mRNA expression, and protein expression were all significantly greater in the 24-h group (<i>p</i> = .0324, <i>p</i> = .0069, <i>p</i> = .0260, respectively), but survivin mRNA and protein expressions were significantly lower than those in the control group (<i>p</i> = .0338, <i>p</i> = .0032, respectively). There was a significant decrease in gastric cancer cells in the miR-34a overexpression group (<i>p</i> = .0020), a significant increase in P53 mRNA and protein expression compared to the control group (<i>p</i> = .0080, <i>p</i> = .0121, respectively), and a significant decrease in survivin mRNA and protein expression compared to the control group. (<i>p</i> = .0213, <i>p</i> = .0069, respectively).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Oxaliplatin inhibits tumor growth, invasion, and metastasis by upregulating miR-34a, activating the expression of the upstream P53 gene, and driving the downregulation of survivin (P53/miR-34a/survivin axis) in BGC-823 gastric cancer cells.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142165746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Meng Jia, Wenli Yuan, Yinqing Chen, Yi Wang, Li Shang, Shisheng Han
Background
The aim of this study was to investigate the association between systemic immune-inflammation index (SII) and all-cause mortality in individuals with chronic kidney disease (CKD).
Patients and Methods
This prospective cohort study was carried out among 9303 participants with CKD from the National Health and Nutrition Examination Survey cycles spanning 1999 to 2018. The mortality data were ascertained by linking participant records to the National Death Index up to December 31, 2019. Complex sampling-weighted multivariate Cox proportional hazards models were employed to estimate the association between SII level and all-cause mortality, providing hazard ratios (HR) and 95% confidence intervals (CI). A restricted cubic spline analysis was conducted to explore potential nonlinear correlation. Subgroup analyses and sensitivity analyses were also conducted.
Results
During a median follow-up period of 86 months, 3400 (36.54%) all-cause deaths were documented. A distinctive “J”-shaped relationship between SII level and all-cause mortality was discerned among individuals with CKD, with the nadir observed at an SII level of 478.93 within the second quartile. After adjusting for potential covariates, the risk of all-cause mortality escalated by 13% per increment of one standard deviation of SII, once SII exceeded 478.93 (HR = 1.13; 95% CI = 1.08–1.18). An elevated SII was associated with an increased risk of all-cause mortality among patients with CKD (Q4 vs. Q2: HR = 1.23; 95% CI = 1.01–1.48). Subgroup analyses indicated that the correlation between SII and CKD mortality was particularly pronounced among participants over 60 years old and individuals with diabetes. Sensitivity analyses revealed a linear positive association between SII and all-cause mortality after removing the extreme 5% outliers of SII.
Conclusions
A distinctive “J”-shaped relationship between SII level and all-cause mortality was identified among individuals with CKD. Further research is warranted to validate and expand upon these findings.
{"title":"Systemic immune inflammation index and all-cause mortality in chronic kidney disease: A prospective cohort study","authors":"Meng Jia, Wenli Yuan, Yinqing Chen, Yi Wang, Li Shang, Shisheng Han","doi":"10.1002/iid3.1358","DOIUrl":"https://doi.org/10.1002/iid3.1358","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The aim of this study was to investigate the association between systemic immune-inflammation index (SII) and all-cause mortality in individuals with chronic kidney disease (CKD).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Patients and Methods</h3>\u0000 \u0000 <p>This prospective cohort study was carried out among 9303 participants with CKD from the National Health and Nutrition Examination Survey cycles spanning 1999 to 2018. The mortality data were ascertained by linking participant records to the National Death Index up to December 31, 2019. Complex sampling-weighted multivariate Cox proportional hazards models were employed to estimate the association between SII level and all-cause mortality, providing hazard ratios (HR) and 95% confidence intervals (CI). A restricted cubic spline analysis was conducted to explore potential nonlinear correlation. Subgroup analyses and sensitivity analyses were also conducted.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>During a median follow-up period of 86 months, 3400 (36.54%) all-cause deaths were documented. A distinctive “J”-shaped relationship between SII level and all-cause mortality was discerned among individuals with CKD, with the nadir observed at an SII level of 478.93 within the second quartile. After adjusting for potential covariates, the risk of all-cause mortality escalated by 13% per increment of one standard deviation of SII, once SII exceeded 478.93 (HR = 1.13; 95% CI = 1.08–1.18). An elevated SII was associated with an increased risk of all-cause mortality among patients with CKD (Q4 vs. Q2: HR = 1.23; 95% CI = 1.01–1.48). Subgroup analyses indicated that the correlation between SII and CKD mortality was particularly pronounced among participants over 60 years old and individuals with diabetes. Sensitivity analyses revealed a linear positive association between SII and all-cause mortality after removing the extreme 5% outliers of SII.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>A distinctive “J”-shaped relationship between SII level and all-cause mortality was identified among individuals with CKD. Further research is warranted to validate and expand upon these findings.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.1358","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142165744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study was designed to evaluate TFAP2A-AS1 expression in the dental pulp of teeth with or without pulpitis and to determine the function of TFAP2A-AS1 in pulp cells.
Methods
GSE92681 was analyzed to filter out differentially expressed lncRNAs. Pulp samples from teeth with pulpitis and healthy teeth (control) were examined using real-time (RT) quantitative polymerase chain reaction (qPCR). Human dental pulp stem cells (hDPSCs) were cultured in a specific medium for osteogenic induction, or treated with lipopolysaccharide (LPS) to simulate inflammation. The viability and apoptosis of human DPSCs (hDPSCs) were determined by XTT assay and apoptosis detection kit. Inflammation was induced by LPS and assessed by measuring the expression and release of inflammatory cytokines after TFAP2A-AS1 knockdown. Osteogenic differentiation of hDPSCs was investigated by determining expression levels of osteogenic markers and alkaline phosphatase (ALP) activity after TFAP2A-AS1 overexpression. The downstream microRNA (miRNA) was predicted. Dual-luciferase reporter was used to confirm the binding between miR-32-5p and TFAP2A-AS1.
Results
The expression of TFAP2A-AS1 was evaluated in inflamed pulp using RT-qPCR. TFAP2A-AS1 had a discriminatory ability for healthy individuals and patients with pulpitis. The expression of TFAP2A-AS1 decreased upon the osteogenic differentiation of hDPSCs, and increased upon the LPS induction. TFAP2A-AS1 can reverse the osteogenic differentiation of hDPSCs, as evidenced by decreased levels of dentine sialophosphoprotein, dentin matrix protein−1, and ALP activity. TFAP2A-AS1 knockdown can promote cell proliferation of hDPSCs and relieve LPS-induced inflammation, as evidenced by decreased levels of TNF-α, IL-1β, and IL-6. miR-32-5p was identified as a downstream miRNA of TFAP2A-AS1.
Conclusion
This study demonstrated the expression and potential function of TFAP2A-AS1 in the human dental pulp. TFAP2A-AS1 can inhibit odontogenic differentiation but promote inflammation in pulp cells.
{"title":"Dysregulation of lncRNA TFAP2A-AS1 is involved in the pathogenesis of pulpitis by the regulation of microRNA-32-5p","authors":"Mingming Liu, Weijing Jia, Lin Bai, Qiaolin Lin","doi":"10.1002/iid3.1312","DOIUrl":"https://doi.org/10.1002/iid3.1312","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study was designed to evaluate TFAP2A-AS1 expression in the dental pulp of teeth with or without pulpitis and to determine the function of TFAP2A-AS1 in pulp cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>GSE92681 was analyzed to filter out differentially expressed lncRNAs. Pulp samples from teeth with pulpitis and healthy teeth (control) were examined using real-time (RT) quantitative polymerase chain reaction (qPCR). Human dental pulp stem cells (hDPSCs) were cultured in a specific medium for osteogenic induction, or treated with lipopolysaccharide (LPS) to simulate inflammation. The viability and apoptosis of human DPSCs (hDPSCs) were determined by XTT assay and apoptosis detection kit. Inflammation was induced by LPS and assessed by measuring the expression and release of inflammatory cytokines after TFAP2A-AS1 knockdown. Osteogenic differentiation of hDPSCs was investigated by determining expression levels of osteogenic markers and alkaline phosphatase (ALP) activity after TFAP2A-AS1 overexpression. The downstream microRNA (miRNA) was predicted. Dual-luciferase reporter was used to confirm the binding between miR-32-5p and TFAP2A-AS1.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The expression of TFAP2A-AS1 was evaluated in inflamed pulp using RT-qPCR. TFAP2A-AS1 had a discriminatory ability for healthy individuals and patients with pulpitis. The expression of TFAP2A-AS1 decreased upon the osteogenic differentiation of hDPSCs, and increased upon the LPS induction. TFAP2A-AS1 can reverse the osteogenic differentiation of hDPSCs, as evidenced by decreased levels of dentine sialophosphoprotein, dentin matrix protein−1, and ALP activity. TFAP2A-AS1 knockdown can promote cell proliferation of hDPSCs and relieve LPS-induced inflammation, as evidenced by decreased levels of TNF-α, IL-1β, and IL-6. miR-32-5p was identified as a downstream miRNA of TFAP2A-AS1.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study demonstrated the expression and potential function of TFAP2A-AS1 in the human dental pulp. TFAP2A-AS1 can inhibit odontogenic differentiation but promote inflammation in pulp cells.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.1312","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142165738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rong Jiang, Haibo Zhou, Long Wen, Xianglong Kong, Zhiguo Zhou
Objective
Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is divided into granulomatosis with polyangiitis (GPA), microscopic polyangiitis, and eosinophilic GPA. It is one of the most severe and potentially fatal autoimmune inflammatory conditions. The etiology and pathology of AAV are complex and poorly understood. Since the onset of the Coronavirus Disease 2019 (COVID-19) pandemic, numerous reports have documented GPA cases following COVID-19, suggesting a potential link between COVID-19 and the development of GPA. This case report discusses a 16-year-old East Asian boy who developed GPA with diffuse alveolar hemorrhage after contracting COVID-19. Additionally, a literature review was conducted to gain a deeper understanding of this disorder.
Methods
The study involved a retrospective analysis of the data of a case of GPA post-COVID-19 infection, aiming to summarize the clinical characteristics of GPA post-COVID-19 infection through a search of databases (PubMed, Wanfang Data, and CNKI), supplemented by standard searches in Google Scholar, Cochrane, Scopus, and LitCovid, and to conduct a comprehensive analysis of the literature.
Results
A total of 12 cases were identified and, when combined with the present case, yielded 13 cases of GPA post-COVID-19 infection, comprising 5 males and 8 females with an average age of (40.6 ± 19.5) years. The interval between COVID-19 infection and the diagnosis of GPA varied from 1 day to 3 months across all cases. Mortality was reported at 7.7% (1/13). The most common clinical manifestations included cough (69.2%) and dyspnea (46.1%). Computed tomography scans revealed ground-glass opacities and multifocal pulmonary nodules. In all cases, positive findings for c-ANCA and protease 3-antibody were observed. Renal involvement was observed in more than half of the patients.
{"title":"COVID-19-induced granulomatosis with polyangiitis: A case report of a 16-year-old East Asian and literature review","authors":"Rong Jiang, Haibo Zhou, Long Wen, Xianglong Kong, Zhiguo Zhou","doi":"10.1002/iid3.70010","DOIUrl":"10.1002/iid3.70010","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is divided into granulomatosis with polyangiitis (GPA), microscopic polyangiitis, and eosinophilic GPA. It is one of the most severe and potentially fatal autoimmune inflammatory conditions. The etiology and pathology of AAV are complex and poorly understood. Since the onset of the Coronavirus Disease 2019 (COVID-19) pandemic, numerous reports have documented GPA cases following COVID-19, suggesting a potential link between COVID-19 and the development of GPA. This case report discusses a 16-year-old East Asian boy who developed GPA with diffuse alveolar hemorrhage after contracting COVID-19. Additionally, a literature review was conducted to gain a deeper understanding of this disorder.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The study involved a retrospective analysis of the data of a case of GPA post-COVID-19 infection, aiming to summarize the clinical characteristics of GPA post-COVID-19 infection through a search of databases (PubMed, Wanfang Data, and CNKI), supplemented by standard searches in Google Scholar, Cochrane, Scopus, and LitCovid, and to conduct a comprehensive analysis of the literature.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 12 cases were identified and, when combined with the present case, yielded 13 cases of GPA post-COVID-19 infection, comprising 5 males and 8 females with an average age of (40.6 ± 19.5) years. The interval between COVID-19 infection and the diagnosis of GPA varied from 1 day to 3 months across all cases. Mortality was reported at 7.7% (1/13). The most common clinical manifestations included cough (69.2%) and dyspnea (46.1%). Computed tomography scans revealed ground-glass opacities and multifocal pulmonary nodules. In all cases, positive findings for c-ANCA and protease 3-antibody were observed. Renal involvement was observed in more than half of the patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142139933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mycobacterium tuberculosis (Mtb), the pathogen responsible for tuberculosis, secretes a multitude of proteins that modulate the host's immune response to ensure its own persistence. The region of difference (RD) genes encoding proteins play key roles in TB immunity and pathogenesis. Nevertheless, the roles of the majority of RD-encoded proteins remain to be elucidated.
Objects
To elucidate the role of Rv2652c located in RD13 in Mtb on bacterial growth, bacterial survival, and host immune response.
Methods
We constructed the strain MS_Rv2652c which over-expresses Mtb RD-encoding protein Rv2652c in M. smegmatis (MS), and compared it with the wild strain in the bacterial growth, bacterial survival, virulence of Rv2652c, and determined the effect of MS_Rv2652c on host immune response in macrophages.
Results
Rv2652c protein is located at cell wall of MS_Rv2652c strain and also an integral component of the Mtb H37Rv cell wall. Rv2652c can enhance the resistance of recombinant MS to various stressors. Moreover, Rv2652c inhibits host proinflammatory responses via modulation of the NF-κB pathway, thereby promoting Mtb survival in vitro and in vivo.
Conclusion
Our data suggest that cell wall protein Rv2652c plays an important role in creating a favorable environment for bacterial survival by modulating host signals and could be established as a potential TB drug target.
{"title":"Mycobacterium tuberculosis protein Rv2652c enhances intracellular survival by inhibiting host immune responses","authors":"Jihong Li, Yafeng Dou","doi":"10.1002/iid3.70012","DOIUrl":"10.1002/iid3.70012","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Backgrounds</h3>\u0000 \u0000 <p><i>Mycobacterium tuberculosis</i> (<i>Mtb</i>), the pathogen responsible for tuberculosis, secretes a multitude of proteins that modulate the host's immune response to ensure its own persistence. The region of difference (RD) genes encoding proteins play key roles in TB immunity and pathogenesis. Nevertheless, the roles of the majority of RD-encoded proteins remain to be elucidated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objects</h3>\u0000 \u0000 <p>To elucidate the role of Rv2652c located in RD13 in Mtb on bacterial growth, bacterial survival, and host immune response.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We constructed the strain MS_Rv2652c which over-expresses <i>Mtb</i> RD-encoding protein Rv2652c in <i>M. smegmatis</i> (MS), and compared it with the wild strain in the bacterial growth, bacterial survival, virulence of Rv2652c, and determined the effect of MS_Rv2652c on host immune response in macrophages.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Rv2652c protein is located at cell wall of MS_Rv2652c strain and also an integral component of the <i>Mtb</i> H37Rv cell wall. Rv2652c can enhance the resistance of recombinant MS to various stressors. Moreover, Rv2652c inhibits host proinflammatory responses via modulation of the NF-κB pathway, thereby promoting <i>Mtb</i> survival in vitro and in vivo.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our data suggest that cell wall protein Rv2652c plays an important role in creating a favorable environment for bacterial survival by modulating host signals and could be established as a potential TB drug target.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142139934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Charles Nkansah, Felix Osei-Boakye, Gabriel Abbam, Samuel K. Appiah, Samira Daud, Bright Boakye, Samsiyatu Abdulai, Madina Ahmed, Theophilus B. Antwi, Birago Boateng, Miigbat P. Libatin, Alexander S. Mensah, Mary K. Missah, Richard V. Duneeh, Ashiya Haruna, Stephany Adda, Pagnaa G. Abdul-Rauf, Zacharia A. Ofori, George B. Fosu, Sandra Segnitome, Isaac Adjei, Emmanuel Appiah-Kubi, Moses Banyeh, Charles A. Derigubah, Muniru M. Tanko, Ejike F. Chukwurah
Background
Severe Plasmodium falciparum malarial anemia is still the principal cause of death in children in underdeveloped countries. An imbalance between proinflammatory and anti-inflammatory cytokines is associated with malaria progression. This study evaluated circulating levels of selected inflammatory cytokines among malaria-infected children in Ghana.
Methods
This case-control study was conducted at Tamale Teaching Hospital, Ghana. One hundred and twenty children with malaria and 60 controls, aged 12−144 months were selected from April to July, 2023 for the study. Malaria was diagnosed through microscopy, full blood count was measured using hematology analyzer, and cytokines were measured using enzyme-linked immunosorbent assay.
Results
Malaria-infected children had higher tumor necrosis factor alpha (TNF-α) (p < .001), interferon-gamma (IFN-ɣ) (p < .001), interleukin (IL)-1β (p < .001), IL-6 (p < .001), granulocyte macrophage-colony stimulating factor (GM-CSF) (p < .001), and IL-10 (p < .001) levels than controls. Participants with high parasitemia had raised TNF-α (p < .001), IFN-ɣ (p < .001), IL-1β (p < .001), IL-6 (p < .001), GM-CSF (p < .001), and IL-10 (p < .001), but reduced IL-3 (p < .001) and TGF-β (p < .001) than those with low parasitemia. Severe malarial anemic children had elevated TNF-α (p < .001), IFN-ɣ (p < .001), IL-1β (p < .001), IL-6 (p < .001), GM-CSF (p < .001), and IL-10 (p < .001), but lower IL-3 (p < .001) and TGF-β (p < .001) than those with uncomplicated malaria.
Conclusion
Parasite density was the principal predictor of the cytokine levels, as parasitemia positively associated with IL-10, GM-CSF, IL-6, IL-1β, IFN-ɣ, and TNF-α, but negatively associated with IL-3 and TGF-β. Malaria is associated with enhanced secretion of pro- and anti-inflammatory cytokines in Ghanaian children. Inflammatory cytokines may be involved in the development of severe malarial anemia in children. However, IL-3 and TGF-β may offer protection against severe malarial anemia.
{"title":"Pro- and anti-inflammatory cytokines mediate the progression of severe anemia in malaria-infected children: A prospective study","authors":"Charles Nkansah, Felix Osei-Boakye, Gabriel Abbam, Samuel K. Appiah, Samira Daud, Bright Boakye, Samsiyatu Abdulai, Madina Ahmed, Theophilus B. Antwi, Birago Boateng, Miigbat P. Libatin, Alexander S. Mensah, Mary K. Missah, Richard V. Duneeh, Ashiya Haruna, Stephany Adda, Pagnaa G. Abdul-Rauf, Zacharia A. Ofori, George B. Fosu, Sandra Segnitome, Isaac Adjei, Emmanuel Appiah-Kubi, Moses Banyeh, Charles A. Derigubah, Muniru M. Tanko, Ejike F. Chukwurah","doi":"10.1002/iid3.70013","DOIUrl":"10.1002/iid3.70013","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Severe <i>Plasmodium falciparum</i> malarial anemia is still the principal cause of death in children in underdeveloped countries. An imbalance between proinflammatory and anti-inflammatory cytokines is associated with malaria progression. This study evaluated circulating levels of selected inflammatory cytokines among malaria-infected children in Ghana.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This case-control study was conducted at Tamale Teaching Hospital, Ghana. One hundred and twenty children with malaria and 60 controls, aged 12−144 months were selected from April to July, 2023 for the study. Malaria was diagnosed through microscopy, full blood count was measured using hematology analyzer, and cytokines were measured using enzyme-linked immunosorbent assay.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Malaria-infected children had higher tumor necrosis factor alpha (TNF-α) (<i>p</i> < .001), interferon-gamma (IFN-ɣ) (<i>p</i> < .001), interleukin (IL)-1β (<i>p</i> < .001), IL-6 (<i>p</i> < .001), granulocyte macrophage-colony stimulating factor (GM-CSF) (<i>p</i> < .001), and IL-10 (<i>p</i> < .001) levels than controls. Participants with high parasitemia had raised TNF-α (<i>p</i> < .001), IFN-ɣ (<i>p</i> < .001), IL-1β (<i>p</i> < .001), IL-6 (<i>p</i> < .001), GM-CSF (<i>p</i> < .001), and IL-10 (<i>p</i> < .001), but reduced IL-3 (<i>p</i> < .001) and TGF-β (<i>p</i> < .001) than those with low parasitemia. Severe malarial anemic children had elevated TNF-α (<i>p</i> < .001), IFN-ɣ (<i>p</i> < .001), IL-1β (<i>p</i> < .001), IL-6 (<i>p</i> < .001), GM-CSF (<i>p</i> < .001), and IL-10 (<i>p</i> < .001), but lower IL-3 (<i>p</i> < .001) and TGF-β (<i>p</i> < .001) than those with uncomplicated malaria.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Parasite density was the principal predictor of the cytokine levels, as parasitemia positively associated with IL-10, GM-CSF, IL-6, IL-1β, IFN-ɣ, and TNF-α, but negatively associated with IL-3 and TGF-β. Malaria is associated with enhanced secretion of pro- and anti-inflammatory cytokines in Ghanaian children. Inflammatory cytokines may be involved in the development of severe malarial anemia in children. However, IL-3 and TGF-β may offer protection against severe malarial anemia.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142139945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jiyun Tian, Shi Chen, Xinzheng Li, Yong Teng, Baobing Chen
Background
This study assesses the prevalence of sexually transmitted infections (STIs) in first time visitors to the STIs clinic in Hangzhou, China, considering different genders, ages and symptoms. And also explores howthe COVID-19 pandemic has affected on STIs.
Methods
From 2019 to 2023, 27,283 first time visitors were tested for nine distinct STIs, including Human Papillomavirus (HPV), Human Immunodeficiency Virus (HIV), syphilis, Herpes Simplex Virus type 2 (HSV-2), Ureaplasma urealyticum (UU), Chlamydia trachomatis (CT), Neisseria gonorrhoeae (NG), Mycoplasma genitalium (MG), and vaginal Candida.
Results
Symptomatic male and female visitors showed overall STI-positive rates of 39.27% and 59.20%, respectively(p < .001). The top three pathogens in both genders were HPV (47.56% and 56.71%), UU (29.21% and 56.47%), and HSV-2 (22.41% and 52.94%). Among asymptomatic visitors, the total STI-positive rate was 36.63% in males and 52.03% in females. Age-stratified analysis revealed higher STI rates in visitors ≤ 20 or >50 years, regardless of gender and symptoms. During the COVID-19 pandemic, symptomatic visitors showed lower positive rates for HPV, HIV, syphilis, and HSV-2, while Candida, UU, CT, NG, and multiple infections increased. Among asymptomatic visitors, HPV had the lowest positive rate, while NG and multiple infections increased during the pandemic.
Conclusion
STI prevalence is notably high, particularly in those aged ≤ 20 and >50 years. It emphasizes the need for enhanced health education, condom use, and vaccination. The COVID-19 pandemic impacting STIs through varied factors, such as reduced sexual activity and clinical service interruption.
{"title":"Prevalence of sexually transmitted infections (STIs) among first time visitors at STIs clinic in Hangzhou, China: Assessing the influence of the COVID-19 pandemic","authors":"Jiyun Tian, Shi Chen, Xinzheng Li, Yong Teng, Baobing Chen","doi":"10.1002/iid3.70009","DOIUrl":"10.1002/iid3.70009","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>This study assesses the prevalence of sexually transmitted infections (STIs) in first time visitors to the STIs clinic in Hangzhou, China, considering different genders, ages and symptoms. And also explores howthe COVID-19 pandemic has affected on STIs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>From 2019 to 2023, 27,283 first time visitors were tested for nine distinct STIs, including <i>Human Papillomavirus</i> (HPV), <i>Human Immunodeficiency Virus</i> (HIV), syphilis, <i>Herpes Simplex Virus type 2</i> (HSV-2), <i>Ureaplasma urealyticum</i> (UU), <i>Chlamydia trachomatis</i> (CT), <i>Neisseria gonorrhoeae</i> (NG), <i>Mycoplasma genitalium</i> (MG), and vaginal Candida.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Symptomatic male and female visitors showed overall STI-positive rates of 39.27% and 59.20%, respectively(<i>p</i> < .001). The top three pathogens in both genders were HPV (47.56% and 56.71%), UU (29.21% and 56.47%), and HSV-2 (22.41% and 52.94%). Among asymptomatic visitors, the total STI-positive rate was 36.63% in males and 52.03% in females. Age-stratified analysis revealed higher STI rates in visitors ≤ 20 or >50 years, regardless of gender and symptoms. During the COVID-19 pandemic, symptomatic visitors showed lower positive rates for HPV, HIV, syphilis, and HSV-2, while Candida, UU, CT, NG, and multiple infections increased. Among asymptomatic visitors, HPV had the lowest positive rate, while NG and multiple infections increased during the pandemic.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>STI prevalence is notably high, particularly in those aged ≤ 20 and >50 years. It emphasizes the need for enhanced health education, condom use, and vaccination. The COVID-19 pandemic impacting STIs through varied factors, such as reduced sexual activity and clinical service interruption.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142106983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Myeloid-derived suppressor cells (MDSCs) play a pivotal role in immunosuppression and tumor progression in hepatocellular carcinoma (HCC). While various treatments like surgical resection, ablation, and radiotherapy have been studied for their effects on circulating MDSC frequencies in HCC patients, the findings remain inconclusive. Transarterial Chemoembolization (TACE) stands as the standard care for unresectable HCC, with Microparticle TACE (mTACE) gaining prominence for its capacity to induce significant tumor necrosis. However, the immunological ramifications of such pathological outcomes are scarcely reported.
Methods and Results
This study aims to elucidate the alterations in MDSC subtypes, specifically monocytic MDSCs (mMDSCs) and early-stage MDSCs (eMDSCs), post-mTACE and to investigate their clinical correlations in HCC patients. A cohort comprising 75 HCC patients, 16 liver cirrhosis patients, and 20 healthy controls (HC) was studied. Peripheral blood samples were collected and analyzed for MDSC subtypes. The study also explored the associations between MDSC frequencies and various clinical parameters in HCC patients. The frequency of mMDSCs was significantly elevated in the HCC group compared to liver cirrhosis and HC. Importantly, mMDSC levels were strongly correlated with aggressive clinical features of HCC, including tumor size, vascular invasion, and distant metastasis. Post-mTACE, a marked reduction in mMDSC frequencies was observed, while eMDSC levels remained stable.
Conclusions
Our findings underscore the critical role of mMDSCs in HCC pathogenesis and their potential as a therapeutic target. The study also highlights the efficacy of mTACE in modulating the immunosuppressive tumor microenvironment, thereby opening new avenues for combinatorial immunotherapeutic strategies in HCC management.
{"title":"Impact of Microparticle Transarterial Chemoembolization (mTACE) on myeloid-derived suppressor cell subtypes in hepatocellular carcinoma: Clinical correlations and therapeutic implications","authors":"Yuanxun Yue, Zhizhong Ren, Yaqin Wang, Ying Liu, Xiaowei Yang, Tianxiao Wang, Yating Bai, He Zhou, Qian Chen, Sujun Li, Yuewei Zhang","doi":"10.1002/iid3.70007","DOIUrl":"10.1002/iid3.70007","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Myeloid-derived suppressor cells (MDSCs) play a pivotal role in immunosuppression and tumor progression in hepatocellular carcinoma (HCC). While various treatments like surgical resection, ablation, and radiotherapy have been studied for their effects on circulating MDSC frequencies in HCC patients, the findings remain inconclusive. Transarterial Chemoembolization (TACE) stands as the standard care for unresectable HCC, with Microparticle TACE (mTACE) gaining prominence for its capacity to induce significant tumor necrosis. However, the immunological ramifications of such pathological outcomes are scarcely reported.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and Results</h3>\u0000 \u0000 <p>This study aims to elucidate the alterations in MDSC subtypes, specifically monocytic MDSCs (mMDSCs) and early-stage MDSCs (eMDSCs), post-mTACE and to investigate their clinical correlations in HCC patients. A cohort comprising 75 HCC patients, 16 liver cirrhosis patients, and 20 healthy controls (HC) was studied. Peripheral blood samples were collected and analyzed for MDSC subtypes. The study also explored the associations between MDSC frequencies and various clinical parameters in HCC patients. The frequency of mMDSCs was significantly elevated in the HCC group compared to liver cirrhosis and HC. Importantly, mMDSC levels were strongly correlated with aggressive clinical features of HCC, including tumor size, vascular invasion, and distant metastasis. Post-mTACE, a marked reduction in mMDSC frequencies was observed, while eMDSC levels remained stable.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our findings underscore the critical role of mMDSCs in HCC pathogenesis and their potential as a therapeutic target. The study also highlights the efficacy of mTACE in modulating the immunosuppressive tumor microenvironment, thereby opening new avenues for combinatorial immunotherapeutic strategies in HCC management.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142106981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To examine the relationship between C-reactive protein (CRP) and knee pain, and further explore whether this association is mediated by obesity.
Methods
The population was derived from 1999 to 2004 National Health and Nutrition Examination Survey. Logistic regression was used to analyze the relationship between CRP and knee pain in three different models, and the linear trend was analyzed. A restricted cubic spline model to assess the nonlinear dose−response relationship between CRP and knee pain. Mediation analyses were used to assess the potential mediating role of obesity. Subgroup analyses and sensitivity analyses were performed to ensure robustness.
Results
Compared with adults with lower CRP (first quartile), those with higher CRP had higher risks of knee pain (odds ratio 1.39, 95% confidence interval 1.12−1.72 in third quartile; 1.56, 1.25−1.95 in fourth quartile) after adjusting for covariates (except body mass index [BMI]), and the proportion mediated by BMI was 76.10% (p < .001). BMI and CRP were linear dose−response correlated with knee pain. The odds ratio for those with obesity compared with normal to knee pain was 2.27 (1.42−3.65) in the first quartile of CRP, 1.99 (1.38−2.86) in the second, 2.15 (1.38−3.33) in the third, and 2.92 (1.72−4.97) in the fourth.
Conclusion
Obesity mediated the systemic inflammation results in knee pain in US adults. Moreover, higher BMI was associated with higher knee pain risk in different degree CRP subgroups, supporting an important role of weight loss in reducing knee pain caused by systemic inflammation.
{"title":"Obesity aggravates the role of C-reactive protein on knee pain: A cross-sectional analysis with NHANES data","authors":"Ling Luo, Mingzi Li, Wenlong Huang, Siying Zhang, Jianbo Sun, Bingsong Zhang, Wei Hu, Haibing Yu","doi":"10.1002/iid3.1371","DOIUrl":"10.1002/iid3.1371","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To examine the relationship between C-reactive protein (CRP) and knee pain, and further explore whether this association is mediated by obesity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The population was derived from 1999 to 2004 National Health and Nutrition Examination Survey. Logistic regression was used to analyze the relationship between CRP and knee pain in three different models, and the linear trend was analyzed. A restricted cubic spline model to assess the nonlinear dose−response relationship between CRP and knee pain. Mediation analyses were used to assess the potential mediating role of obesity. Subgroup analyses and sensitivity analyses were performed to ensure robustness.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Compared with adults with lower CRP (first quartile), those with higher CRP had higher risks of knee pain (odds ratio 1.39, 95% confidence interval 1.12−1.72 in third quartile; 1.56, 1.25−1.95 in fourth quartile) after adjusting for covariates (except body mass index [BMI]), and the proportion mediated by BMI was 76.10% (<i>p</i> < .001). BMI and CRP were linear dose−response correlated with knee pain. The odds ratio for those with obesity compared with normal to knee pain was 2.27 (1.42−3.65) in the first quartile of CRP, 1.99 (1.38−2.86) in the second, 2.15 (1.38−3.33) in the third, and 2.92 (1.72−4.97) in the fourth.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Obesity mediated the systemic inflammation results in knee pain in US adults. Moreover, higher BMI was associated with higher knee pain risk in different degree CRP subgroups, supporting an important role of weight loss in reducing knee pain caused by systemic inflammation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.1371","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142106982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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