Objectives: Resveratrol has been implicated in the differentiation and development of human umbilical cord mesenchymal stem cells. The differentiation of into esophageal fibroblasts is a promising strategy for esophageal tissue engineering. However, the pharmacological effect and underlying mechanism of resveratrol on human umbilical cord mesenchymal stem cells differentiation are unknown. Here, we investigated the effects and mechanism of resveratrol on the differentiation of human umbilical cord mesenchymal stem cells. Methods: Using a transwell-membrane coculture system to culture human umbilical cord mesenchymal stem cells and esophageal fibroblasts, we examined how resveratrol act on the differentiation of human umbilical cord mesenchymal stem cells. Immunocytochemistry, Sirius red staining, quantitative real-time PCR, and Western blotting were performed to examine collagen synthesis and possible signaling pathways in human umbilical cord mesenchymal stem cells. Results: We found that resveratrol promoted collagen synthesis and AKT phosphorylation. However, co-treatment of cells with resveratrol and the PI3K inhibitor LY294002 inhibited collagen synthesis and AKT phosphorylation. We demonstrated that resveratrol down-regulated the expression of IL-6, TGF-β, caspase-9, and Bax by activating the AKT pathway in human umbilical cord mesenchymal stem cell. Furthermore, resveratrol inhibited phosphorylated NF-ĸB in human umbilical cord mesenchymal stem cells. Conclusion: Our data suggest that resveratrol promotes the differentiation of human umbilical cord mesenchymal stem cells into fibroblasts. The underlying mechanism is associated with the downregulation of IL-6 and TGF-β via the AKT pathway and by inhibiting the NF-ĸB pathway. Resveratrol may be useful for esophageal tissue engineering.
{"title":"Resveratrol promotes the differentiation of human umbilical cord mesenchymal stem cells into esophageal fibroblasts via AKT signaling pathway","authors":"Xiujing Chen, Zihao Sun, Qian Wu, Lijuan Shao, Jiaxin Bei, Yiguang Lin, Hongjie Chen, Size Chen","doi":"10.1177/03946320241249397","DOIUrl":"https://doi.org/10.1177/03946320241249397","url":null,"abstract":"Objectives: Resveratrol has been implicated in the differentiation and development of human umbilical cord mesenchymal stem cells. The differentiation of into esophageal fibroblasts is a promising strategy for esophageal tissue engineering. However, the pharmacological effect and underlying mechanism of resveratrol on human umbilical cord mesenchymal stem cells differentiation are unknown. Here, we investigated the effects and mechanism of resveratrol on the differentiation of human umbilical cord mesenchymal stem cells. Methods: Using a transwell-membrane coculture system to culture human umbilical cord mesenchymal stem cells and esophageal fibroblasts, we examined how resveratrol act on the differentiation of human umbilical cord mesenchymal stem cells. Immunocytochemistry, Sirius red staining, quantitative real-time PCR, and Western blotting were performed to examine collagen synthesis and possible signaling pathways in human umbilical cord mesenchymal stem cells. Results: We found that resveratrol promoted collagen synthesis and AKT phosphorylation. However, co-treatment of cells with resveratrol and the PI3K inhibitor LY294002 inhibited collagen synthesis and AKT phosphorylation. We demonstrated that resveratrol down-regulated the expression of IL-6, TGF-β, caspase-9, and Bax by activating the AKT pathway in human umbilical cord mesenchymal stem cell. Furthermore, resveratrol inhibited phosphorylated NF-ĸB in human umbilical cord mesenchymal stem cells. Conclusion: Our data suggest that resveratrol promotes the differentiation of human umbilical cord mesenchymal stem cells into fibroblasts. The underlying mechanism is associated with the downregulation of IL-6 and TGF-β via the AKT pathway and by inhibiting the NF-ĸB pathway. Resveratrol may be useful for esophageal tissue engineering.","PeriodicalId":14046,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"44 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140836688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-30DOI: 10.1177/03946320241249395
Rong Huang, Xiaoxu Lu, Xueming Sun, Hui Wu
Background: Glioblastoma, a highly aggressive brain tumor, poses a significant clinical challenge, particularly in the context of radiotherapy. In this study, we aimed to explore infiltrating immune cells and identify immune-related genes associated with glioblastoma radiotherapy prognosis. Subsequently, we constructed a signature based on these genes to discern differences in molecular and tumor microenvironment immune characteristics, ultimately informing potential therapeutic strategies for patients with varying risk profiles. Methods: We leveraged UCSC Xena and CGGA gene expression profiles from post-radiotherapy glioblastoma as verification cohorts. Infiltration ratios were stratified into high and low groups based on the median value. Differential gene expression was determined through Limma differential analysis. A signature comprising four genes was constructed, guided by Gene Ontology (GO) functional enrichment results and Kaplan–Meier survival analysis. We evaluated differences in cell infiltration levels, Immune Score, Stromal Score, and ESTIMATE Score and their Pearson correlations with the signature. Spearman’s correlation was computed between the signature and patient drug sensitivity (IC50), predicted using Genomics of Drug Sensitivity in Cancer (GDSC) and CCLE databases. Results: Notably, the infiltration of central memory CD8+T cells exhibited a significant correlation with glioblastoma radiotherapy prognosis. Samples were dichotomized into high- and low-risk groups based on the optimal signature threshold (2.466642). Kaplan–Meier (K-M) survival analysis revealed that the high-risk group experienced a significantly poorer prognosis ( p = .0068), with AUC values exceeding 0.82 at 1, 3, and 5 years, underscoring the robust predictive potential of the signature scoring system. Independent validation sets substantiated the validity of the signature. Statistically significant differences in tumor microenvironments (p < .05) were observed between high- and low-risk groups, and these differences were significantly correlated with the signature ( p < .05). Furthermore, there were significant correlations between high and low-risk groups regarding immune checkpoint expressions, Immune Prognostic Score (IPS), and Tumor Immune Dysfunction and Exclusion (TIDE) scores. Conclusion: The immune cell signature, comprising SDC-1, PLAUR, FN1, and CXCL13, holds promise as a predictive tool for assessing glioblastoma prognosis following radiotherapy. This signature also offers valuable guidance for tailoring treatment strategies, emphasizing its potential clinical relevance in improving patient outcomes.
{"title":"A novel immune cell signature for predicting glioblastoma after radiotherapy prognosis and guiding therapy","authors":"Rong Huang, Xiaoxu Lu, Xueming Sun, Hui Wu","doi":"10.1177/03946320241249395","DOIUrl":"https://doi.org/10.1177/03946320241249395","url":null,"abstract":"Background: Glioblastoma, a highly aggressive brain tumor, poses a significant clinical challenge, particularly in the context of radiotherapy. In this study, we aimed to explore infiltrating immune cells and identify immune-related genes associated with glioblastoma radiotherapy prognosis. Subsequently, we constructed a signature based on these genes to discern differences in molecular and tumor microenvironment immune characteristics, ultimately informing potential therapeutic strategies for patients with varying risk profiles. Methods: We leveraged UCSC Xena and CGGA gene expression profiles from post-radiotherapy glioblastoma as verification cohorts. Infiltration ratios were stratified into high and low groups based on the median value. Differential gene expression was determined through Limma differential analysis. A signature comprising four genes was constructed, guided by Gene Ontology (GO) functional enrichment results and Kaplan–Meier survival analysis. We evaluated differences in cell infiltration levels, Immune Score, Stromal Score, and ESTIMATE Score and their Pearson correlations with the signature. Spearman’s correlation was computed between the signature and patient drug sensitivity (IC50), predicted using Genomics of Drug Sensitivity in Cancer (GDSC) and CCLE databases. Results: Notably, the infiltration of central memory CD8+T cells exhibited a significant correlation with glioblastoma radiotherapy prognosis. Samples were dichotomized into high- and low-risk groups based on the optimal signature threshold (2.466642). Kaplan–Meier (K-M) survival analysis revealed that the high-risk group experienced a significantly poorer prognosis ( p = .0068), with AUC values exceeding 0.82 at 1, 3, and 5 years, underscoring the robust predictive potential of the signature scoring system. Independent validation sets substantiated the validity of the signature. Statistically significant differences in tumor microenvironments (p < .05) were observed between high- and low-risk groups, and these differences were significantly correlated with the signature ( p < .05). Furthermore, there were significant correlations between high and low-risk groups regarding immune checkpoint expressions, Immune Prognostic Score (IPS), and Tumor Immune Dysfunction and Exclusion (TIDE) scores. Conclusion: The immune cell signature, comprising SDC-1, PLAUR, FN1, and CXCL13, holds promise as a predictive tool for assessing glioblastoma prognosis following radiotherapy. This signature also offers valuable guidance for tailoring treatment strategies, emphasizing its potential clinical relevance in improving patient outcomes.","PeriodicalId":14046,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"60 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140836974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-30DOI: 10.1177/03946320241250294
Menha Swellam, Mohamed K. Khalifa, Amira M Nageeb, Lobna Ezz El-Arab, Manal El-Mahdy, Khaled El-Bahy, Magda Sayed Mahmoud
Objectives: Gliobalstoma is the most common primary brain tumor in adults with an extensive genetic and transcriptional heterogeneity, still identification of the role of DNA methylation, as one of epigenetic alterations, is emerged. Authors aimed to study the clinical role of N-myc downstream-regulated gene 2 (NDRG2) –based methylation among GBM patients versus benign neurological diseases (BND), investigate its prognostic role and its relation with survival outcomes. Methods: A total of 78 FFPE specimens were recruited as follows: GBM ( n = 58) and BND ( n = 20) then analyzed for NDRG2 methylation using Methyl II quantitative PCR system. The sensitivity and specificity of methylation was detected using receiver operating characteristic (ROC) curve and the relation with clinicopathological criteria for GBM and response to treatment were studied. Survival patterns; progression free survival (PFS) and overall survival (OS) were analyzed using Kaplan-Meier analyses. Results: Mean methylation NDRG2 level was significantly increased in GBM patients as compared to BND and its sensitivity and specificity were 96.55% and 95%, respectively with area under curve (AUC) equals 0.973. Among the clinical characteristic factors, mean methylation level reported significant difference with ECOG and tumor site. Survival out comes revealed that NDRG2 methylation increased with worse PFS and OS at significant level (long rank test X 2 = 13.3, p < .0001; and X 2 = 7.1, p = .008, respectively). Conclusion: Current findings highlight the importance of studying DNA methylation of NDRG2 as a key factor to understand the role of epigenetic alterations in GBM.
{"title":"Clinical role of NDRG2-based methylation status on survival pattern of glioblastoma","authors":"Menha Swellam, Mohamed K. Khalifa, Amira M Nageeb, Lobna Ezz El-Arab, Manal El-Mahdy, Khaled El-Bahy, Magda Sayed Mahmoud","doi":"10.1177/03946320241250294","DOIUrl":"https://doi.org/10.1177/03946320241250294","url":null,"abstract":"Objectives: Gliobalstoma is the most common primary brain tumor in adults with an extensive genetic and transcriptional heterogeneity, still identification of the role of DNA methylation, as one of epigenetic alterations, is emerged. Authors aimed to study the clinical role of N-myc downstream-regulated gene 2 (NDRG2) –based methylation among GBM patients versus benign neurological diseases (BND), investigate its prognostic role and its relation with survival outcomes. Methods: A total of 78 FFPE specimens were recruited as follows: GBM ( n = 58) and BND ( n = 20) then analyzed for NDRG2 methylation using Methyl II quantitative PCR system. The sensitivity and specificity of methylation was detected using receiver operating characteristic (ROC) curve and the relation with clinicopathological criteria for GBM and response to treatment were studied. Survival patterns; progression free survival (PFS) and overall survival (OS) were analyzed using Kaplan-Meier analyses. Results: Mean methylation NDRG2 level was significantly increased in GBM patients as compared to BND and its sensitivity and specificity were 96.55% and 95%, respectively with area under curve (AUC) equals 0.973. Among the clinical characteristic factors, mean methylation level reported significant difference with ECOG and tumor site. Survival out comes revealed that NDRG2 methylation increased with worse PFS and OS at significant level (long rank test X<jats:sup> 2</jats:sup> = 13.3, p < .0001; and X<jats:sup> 2</jats:sup> = 7.1, p = .008, respectively). Conclusion: Current findings highlight the importance of studying DNA methylation of NDRG2 as a key factor to understand the role of epigenetic alterations in GBM.","PeriodicalId":14046,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"4 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140836703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background and objectivesMetformin, an oral hypoglycemic drug, has been suggested to possess antitumour activity in several types of cancers. Additionally, interleukin-8 (IL-8) has been reported to be involved in the development and metastasis of many cancers. However, the effect of metformin on IL-8 expression in hepatocellular carcinoma (HCC) remains unclear. Therefore, this study aimed to investigate whether metformin could inhibit IL-8 expression to exert an inhibitory effect on HCC progression.Materials and methodsThe IL-8 levels were measured in the plasma of 159 HCC patients (86 men, 73 women; average age 56 years) and in the culture supernatant of HCC cells (Hep3B and HuH7) using flow cytometry. In addition, the protein expression levels of IL-8 were also validated by the Human Protein Atlas (HPA) database. The prognostic value of IL-8 was evaluated using the Kaplan–Meier Plotter database. The association between IL-8 expression and immune checkpoints was estimated using the TIMER and The Cancer Genome Atlas (TCGA) databases. What’s more, bioinformatics analysis, western blotting, and transwell assays were conducted to illustrate the molecular mechanism of metformin (≤1 mM) on IL-8 in HCC.ResultsIL-8 expression was found to be increased in the plasma of HCC patients, which is consistent with the expression of IL-8 in HCC cells and tissues. High expression of IL-8 was significantly related to poor prognosis. In addition, IL-8 was positively correlated with immune checkpoints in HCC. Notably, we found that low-dose metformin could inhibit the secretion of IL-8 by HCC cells and the migration of HCC cells. Mechanistically, low-dose metformin significantly suppresses HCC metastasis mainly through the AMPK/JNK/IL-8/MMP9 pathway.ConclusionThe results indicate that low-dose metformin can inhibit HCC metastasis by suppressing IL-8 expression. Targeting the AMPK/JNK/IL-8 axis may be a promising treatment strategy for patients with HCC metastasis.
{"title":"Low-dose metformin suppresses hepatocellular carcinoma metastasis via the AMPK/JNK/IL-8 pathway","authors":"Chengwen Zhao, Lu Zheng, Yuting Ma, Yue Zhang, Chanjuan Yue, Feng Gu, Guoping Niu, Yongqiang Chen","doi":"10.1177/03946320241249445","DOIUrl":"https://doi.org/10.1177/03946320241249445","url":null,"abstract":"Background and objectivesMetformin, an oral hypoglycemic drug, has been suggested to possess antitumour activity in several types of cancers. Additionally, interleukin-8 (IL-8) has been reported to be involved in the development and metastasis of many cancers. However, the effect of metformin on IL-8 expression in hepatocellular carcinoma (HCC) remains unclear. Therefore, this study aimed to investigate whether metformin could inhibit IL-8 expression to exert an inhibitory effect on HCC progression.Materials and methodsThe IL-8 levels were measured in the plasma of 159 HCC patients (86 men, 73 women; average age 56 years) and in the culture supernatant of HCC cells (Hep3B and HuH7) using flow cytometry. In addition, the protein expression levels of IL-8 were also validated by the Human Protein Atlas (HPA) database. The prognostic value of IL-8 was evaluated using the Kaplan–Meier Plotter database. The association between IL-8 expression and immune checkpoints was estimated using the TIMER and The Cancer Genome Atlas (TCGA) databases. What’s more, bioinformatics analysis, western blotting, and transwell assays were conducted to illustrate the molecular mechanism of metformin (≤1 mM) on IL-8 in HCC.ResultsIL-8 expression was found to be increased in the plasma of HCC patients, which is consistent with the expression of IL-8 in HCC cells and tissues. High expression of IL-8 was significantly related to poor prognosis. In addition, IL-8 was positively correlated with immune checkpoints in HCC. Notably, we found that low-dose metformin could inhibit the secretion of IL-8 by HCC cells and the migration of HCC cells. Mechanistically, low-dose metformin significantly suppresses HCC metastasis mainly through the AMPK/JNK/IL-8/MMP9 pathway.ConclusionThe results indicate that low-dose metformin can inhibit HCC metastasis by suppressing IL-8 expression. Targeting the AMPK/JNK/IL-8 axis may be a promising treatment strategy for patients with HCC metastasis.","PeriodicalId":14046,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"2012 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140836671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-23DOI: 10.1177/03946320241234736
Feng Zhan, Jun Zhang, Ping He, Wenteng Chen, Yanhong Ouyang
Sepsis, critical condition marked by severe organ dysfunction from uncontrolled infection, involves the endothelium significantly. Macrophages, through paracrine actions, play a vital role in sepsis, but their mechanisms in sepsis pathogenesis remain elusive. Objective: We aimed to explore how macrophage-derived exosomes with low miR-141 expression promote pyroptosis in endothelial cells (ECs). Exosomes from THP-1 cell supernatant were isolated and characterized. The effects of miR-141 mimic/inhibitor on apoptosis, proliferation, and invasion of Human Umbilical Vein Endothelial Cells (HUVECs) were assessed using flow cytometry, CCK-8, and transwell assays. Key pyroptosis-related proteins, including caspase-1, IL-18, IL-1β, NLR Family Pyrin Domain Containing 3 (NLRP3), ASC, and cleaved-GSDMD, were analyzed via Western blot. The interaction between miR-141 and NLRP3 was studied using RNAhybrid v2.2 and dual-Luciferase reporter assays. The mRNA and protein level of NLRP3 after exosomal miR-141 inhibitor treatment was detected by qPCR and Western blot, respectively. Exosomes were successfully isolated. miR-141 mimic reduced cell death and pyroptosis-related protein expression in HUVECs, while the inhibitor had opposite effects, increasing cell death, and enhancing pyroptosis protein expression. Additionally, macrophage-derived exosomal miR-141 inhibitor increased cell death and pyroptosis-related proteins in HUVECs. miR-141 inhibits NLRP3 transcription. Macrophages facilitate sepsis progression by secreting miR-141 decreased exosomes to activate NLRP3-mediated pyroptosis in ECs, which could be a potentially valuable target of sepsis therapy.
{"title":"Macrophage-derived exosomal miRNA-141 triggers endothelial cell pyroptosis by targeting NLRP3 to accelerate sepsis progression","authors":"Feng Zhan, Jun Zhang, Ping He, Wenteng Chen, Yanhong Ouyang","doi":"10.1177/03946320241234736","DOIUrl":"https://doi.org/10.1177/03946320241234736","url":null,"abstract":"Sepsis, critical condition marked by severe organ dysfunction from uncontrolled infection, involves the endothelium significantly. Macrophages, through paracrine actions, play a vital role in sepsis, but their mechanisms in sepsis pathogenesis remain elusive. Objective: We aimed to explore how macrophage-derived exosomes with low miR-141 expression promote pyroptosis in endothelial cells (ECs). Exosomes from THP-1 cell supernatant were isolated and characterized. The effects of miR-141 mimic/inhibitor on apoptosis, proliferation, and invasion of Human Umbilical Vein Endothelial Cells (HUVECs) were assessed using flow cytometry, CCK-8, and transwell assays. Key pyroptosis-related proteins, including caspase-1, IL-18, IL-1β, NLR Family Pyrin Domain Containing 3 (NLRP3), ASC, and cleaved-GSDMD, were analyzed via Western blot. The interaction between miR-141 and NLRP3 was studied using RNAhybrid v2.2 and dual-Luciferase reporter assays. The mRNA and protein level of NLRP3 after exosomal miR-141 inhibitor treatment was detected by qPCR and Western blot, respectively. Exosomes were successfully isolated. miR-141 mimic reduced cell death and pyroptosis-related protein expression in HUVECs, while the inhibitor had opposite effects, increasing cell death, and enhancing pyroptosis protein expression. Additionally, macrophage-derived exosomal miR-141 inhibitor increased cell death and pyroptosis-related proteins in HUVECs. miR-141 inhibits NLRP3 transcription. Macrophages facilitate sepsis progression by secreting miR-141 decreased exosomes to activate NLRP3-mediated pyroptosis in ECs, which could be a potentially valuable target of sepsis therapy.","PeriodicalId":14046,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"3 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140804991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: This retrospective study investigates the influence of overweight and obesity status on pulmonary function, airway inflammatory markers, and airway responsiveness in elderly asthma patients. Methods: Patients with asthma older than 65 years old who completed a bronchial provocation test (BPT) or bronchial dilation test (BDT) and a fractional exhaled nitric oxide (FeNO) test between December 2015 and June 2020 were identified retrospectively for this study. All of the patients were categorized into overweight/obesity and non-obesity groups based on their BMI. Pulmonary function test (PFT) and FeNO measurements were accomplished according to the 2014 recommendations of the Chinese National Guidelines of Pulmonary Function Test and American Thoracic Society/European Respiratory Society recommendations, respectively. Results: A total of 136 patients with an average age of 71.2 ± 5.40 years were identified. The average BMI was 23.8 ± 3.63, while the value of FeNO was 42.3 ± 38.4 parts per billion (ppb). In contrast to the non-obesity group, which had a value of 48.8 ± 43.1 ppb for FeNO, the overweight/obesity group had a significant lower value of 35.4 ± 31.4 ppb. There was no significant difference in the proportion of individuals with high airway hyperresponsiveness between the overweight/obesity and non-obesity groups (96 patients in total). Multiple linear regression analysis established an inverse correlation between FeNO and Provocation concentration causing a 20% fall in FEV1(PC20) but excluded significant relationships with age and BMI. The model’s R is 0.289, and its p value is 0.045. Conclusion: The elderly Chinese Han asthmatics with overweight/obesity had lower FeNO levels than those with non-obese according to our findings. In addition, the FeNO level was inversely correlated between FeNO levels and PC20 in elderly asthmatics.
{"title":"Effect of overweight/obesity on relationship between fractional exhaled nitric oxide and airway hyperresponsiveness in Chinese elderly patients with asthma","authors":"Fengjia Chen, Yangli Liu, Long-hua Sun, Zhimin Zeng, Xinyan Huang","doi":"10.1177/03946320241246713","DOIUrl":"https://doi.org/10.1177/03946320241246713","url":null,"abstract":"Purpose: This retrospective study investigates the influence of overweight and obesity status on pulmonary function, airway inflammatory markers, and airway responsiveness in elderly asthma patients. Methods: Patients with asthma older than 65 years old who completed a bronchial provocation test (BPT) or bronchial dilation test (BDT) and a fractional exhaled nitric oxide (FeNO) test between December 2015 and June 2020 were identified retrospectively for this study. All of the patients were categorized into overweight/obesity and non-obesity groups based on their BMI. Pulmonary function test (PFT) and FeNO measurements were accomplished according to the 2014 recommendations of the Chinese National Guidelines of Pulmonary Function Test and American Thoracic Society/European Respiratory Society recommendations, respectively. Results: A total of 136 patients with an average age of 71.2 ± 5.40 years were identified. The average BMI was 23.8 ± 3.63, while the value of FeNO was 42.3 ± 38.4 parts per billion (ppb). In contrast to the non-obesity group, which had a value of 48.8 ± 43.1 ppb for FeNO, the overweight/obesity group had a significant lower value of 35.4 ± 31.4 ppb. There was no significant difference in the proportion of individuals with high airway hyperresponsiveness between the overweight/obesity and non-obesity groups (96 patients in total). Multiple linear regression analysis established an inverse correlation between FeNO and Provocation concentration causing a 20% fall in FEV<jats:sub>1</jats:sub>(PC20) but excluded significant relationships with age and BMI. The model’s R is 0.289, and its p value is 0.045. Conclusion: The elderly Chinese Han asthmatics with overweight/obesity had lower FeNO levels than those with non-obese according to our findings. In addition, the FeNO level was inversely correlated between FeNO levels and PC20 in elderly asthmatics.","PeriodicalId":14046,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"17 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140635777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-04-13DOI: 10.1177/03946320100230s101
A. Varricchio, F. Avvisati, A.M. Varricchio, G. Tortoriello, G. Ciprandi
The airways should be considered as a functional unit. Indeed, disorders involving the upper respiratory tract (URT) spread to the lower respiratory tract (LRT). Modern functional anatomy divides U...
{"title":"The Nose and Paranasal Sinuses","authors":"A. Varricchio, F. Avvisati, A.M. Varricchio, G. Tortoriello, G. Ciprandi","doi":"10.1177/03946320100230s101","DOIUrl":"https://doi.org/10.1177/03946320100230s101","url":null,"abstract":"The airways should be considered as a functional unit. Indeed, disorders involving the upper respiratory tract (URT) spread to the lower respiratory tract (LRT). Modern functional anatomy divides U...","PeriodicalId":14046,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"79 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2023-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138527657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-05-01DOI: 10.1177/03946320221101287
Haijun Liu, Qianhua Li, Xiu-ning Wei, Jian-da Ma, K. Long, Xia Ouyang, Nemin Liu, Yongsheng Li, L. He, L. Dai, Xiaoyan Cai
Background: Systemic lupus erythematosus (SLE) commonly occurs in premenopausal women and is associated with elevated estrogen levels. Patients with SLE may have abnormal serum triglyceride (TG) levels, and lipid reportedly promotes kidney damage in patients with nephrosis. Since estrogen regulates lipid levels, we investigated the serum lipid levels of premenopausal women with SLE and their relationship with proteinuria. Methods: This cross-sectional study included 123 premenopausal women with SLE (SLE group), who were classified into 24-h urine protein exceeding 0.5 g (24 h-UPRO > 0.5 g, n = 22) and 24 h-UPRO ≤ 0.5 g (n = 101) subgroups, and 100 similarly aged healthy women (control group). Clinical characteristics and biomarker levels were compared between these groups. The associated factors of proteinuria over 0.5 g/day were evaluated using multivariate logistic regression. A receiver operating characteristic (ROC) curve was plotted to assess the cholesterol (CH) cut-off associated with increased development of proteinuria over 0.5 g/day. Results: The SLE group had significantly higher serum TG levels than that of control group. 24 h-UPRO were significantly correlated with serum creatinine, CH, TG, and uric acid levels. Serum CH level was the greatest associated factor for proteinuria over 0.5 g/day. The area under the ROC curve was 0.843, with a CH cut-off of 4.58 mmol/L. Patients with serum CH above 4.58 mmol/L had a higher proportion of type IV LN, but with no statistical difference. Conclusions: In premenopausal SLE patients, serum TG levels were higher than in healthy women, and serum CH levels were the primary associated factor for proteinuria over 0.5 g/day. Proteinura over 0.5 g/day may occur in women with SLE with serum CH levels >4.58 mmol/L. CH levels may be useful for predicting proteinuria.
背景:系统性红斑狼疮(SLE)常见于绝经前妇女，与雌激素水平升高有关。SLE患者可能有异常的血清甘油三酯(TG)水平，据报道，脂质会促进肾病患者的肾脏损害。由于雌激素调节脂质水平，我们研究了绝经前SLE妇女的血脂水平及其与蛋白尿的关系。方法:本横断研究纳入123例绝经前SLE女性(SLE组)，分为24 h尿蛋白超过0.5 g (24 h-UPRO低于0.5 g, n = 22)和24 h-UPRO≤0.5 g (n = 101)亚组，以及100例年龄相似的健康女性(对照组)。比较两组的临床特征和生物标志物水平。蛋白尿超过0.5 g/d的相关因素采用多因素logistic回归进行评估。绘制受试者工作特征(ROC)曲线，以评估胆固醇(CH)临界值与蛋白尿发生率超过0.5 g/天相关。结果:SLE组血清TG水平明显高于对照组。24 h-UPRO与血清肌酐、CH、TG、尿酸水平显著相关。血清CH水平是蛋白尿超过0.5 g/d的最大相关因素。ROC曲线下面积为0.843,CH截止值为4.58 mmol/L。血清CH > 4.58 mmol/L的患者发生IV型LN的比例较高，但差异无统计学意义。结论:绝经前SLE患者血清TG水平高于健康女性，血清CH水平是蛋白尿超过0.5 g/d的主要相关因素。蛋白尿超过0.5 g/天可能发生在血清CH水平为bb0 4.58 mmol/L的SLE患者。CH水平可用于预测蛋白尿。
{"title":"Elevated serum cholesterol levels are associated with proteinuria over 0.5 g/day in premenopausal women with systemic lupus erythematosus","authors":"Haijun Liu, Qianhua Li, Xiu-ning Wei, Jian-da Ma, K. Long, Xia Ouyang, Nemin Liu, Yongsheng Li, L. He, L. Dai, Xiaoyan Cai","doi":"10.1177/03946320221101287","DOIUrl":"https://doi.org/10.1177/03946320221101287","url":null,"abstract":"Background: Systemic lupus erythematosus (SLE) commonly occurs in premenopausal women and is associated with elevated estrogen levels. Patients with SLE may have abnormal serum triglyceride (TG) levels, and lipid reportedly promotes kidney damage in patients with nephrosis. Since estrogen regulates lipid levels, we investigated the serum lipid levels of premenopausal women with SLE and their relationship with proteinuria. Methods: This cross-sectional study included 123 premenopausal women with SLE (SLE group), who were classified into 24-h urine protein exceeding 0.5 g (24 h-UPRO > 0.5 g, n = 22) and 24 h-UPRO ≤ 0.5 g (n = 101) subgroups, and 100 similarly aged healthy women (control group). Clinical characteristics and biomarker levels were compared between these groups. The associated factors of proteinuria over 0.5 g/day were evaluated using multivariate logistic regression. A receiver operating characteristic (ROC) curve was plotted to assess the cholesterol (CH) cut-off associated with increased development of proteinuria over 0.5 g/day. Results: The SLE group had significantly higher serum TG levels than that of control group. 24 h-UPRO were significantly correlated with serum creatinine, CH, TG, and uric acid levels. Serum CH level was the greatest associated factor for proteinuria over 0.5 g/day. The area under the ROC curve was 0.843, with a CH cut-off of 4.58 mmol/L. Patients with serum CH above 4.58 mmol/L had a higher proportion of type IV LN, but with no statistical difference. Conclusions: In premenopausal SLE patients, serum TG levels were higher than in healthy women, and serum CH levels were the primary associated factor for proteinuria over 0.5 g/day. Proteinura over 0.5 g/day may occur in women with SLE with serum CH levels >4.58 mmol/L. CH levels may be useful for predicting proteinuria.","PeriodicalId":14046,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47546206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objectives Glioma is a common type of brain tumor with high incidence and mortality rates. Procollagen C-protease enhancer protein (PCOLCE) has been shown to regulate tumor growth and metastasis in several cancers. However, the role of PCOLCE in glioma is unknown. This study aims to assess the association between PCOLCE and prognosis of glioma, and investigated the potential mechanisms. Methods The prognostic value of PCOLCE was determined using data from nine publicly available glioma cohorts. We also investigated the relationship between PCOLCE and glioma immune microenvironment and predicted response to immunotherapy based on the expression levels of PCOLCE. The potential roles of PCOLCE in glioma were also explored and validated in cell experiment. Results Survival analysis suggested that high-PCOLCE expression was associated with poor prognosis in glioma. Upregulation of PCOLCE enhanced an immune suppressive microenvironment in glioma by regulating immunocyte infiltration and Cancer-Immunity Cycle. Cox and ROC analysis revealed that PCOLCE was a prognostic factor for glioma and could be used to predict survival of the patients. Patients with low-PCOLCE expression were more likely to respond to Immunotherapy with ICI (immune checkpoint inhibitor) and survive longer. Enrichment analysis showed that PCOLCE was associated with multiple tumor-related pathways. Finally, we demonstrated that the knockdown of PCOLCE inhibited glioma development by regulating cell cycle and promoting apoptosis in in vitro experiments. Conclusion PCOLCE promotes glioma progression by regulating multiple tumor-related pathways and immune microenvironment and can be used as a prognostic factor for glioma.
{"title":"Procollagen C-protease enhancer protein is a prognostic factor for glioma and promotes glioma development by regulating multiple tumor-related pathways and immune microenvironment","authors":"Zijun Zhao, Jiahui Zhao, Zairan Wang, Yue Wu, Zhanzhan Zhang, Zihan Song, Jihao Miao, Boheng Liu, Shiyang Zhang, Boyu Sun, Zongmao Zhao","doi":"10.1177/03946320221104548","DOIUrl":"https://doi.org/10.1177/03946320221104548","url":null,"abstract":"Objectives Glioma is a common type of brain tumor with high incidence and mortality rates. Procollagen C-protease enhancer protein (PCOLCE) has been shown to regulate tumor growth and metastasis in several cancers. However, the role of PCOLCE in glioma is unknown. This study aims to assess the association between PCOLCE and prognosis of glioma, and investigated the potential mechanisms. Methods The prognostic value of PCOLCE was determined using data from nine publicly available glioma cohorts. We also investigated the relationship between PCOLCE and glioma immune microenvironment and predicted response to immunotherapy based on the expression levels of PCOLCE. The potential roles of PCOLCE in glioma were also explored and validated in cell experiment. Results Survival analysis suggested that high-PCOLCE expression was associated with poor prognosis in glioma. Upregulation of PCOLCE enhanced an immune suppressive microenvironment in glioma by regulating immunocyte infiltration and Cancer-Immunity Cycle. Cox and ROC analysis revealed that PCOLCE was a prognostic factor for glioma and could be used to predict survival of the patients. Patients with low-PCOLCE expression were more likely to respond to Immunotherapy with ICI (immune checkpoint inhibitor) and survive longer. Enrichment analysis showed that PCOLCE was associated with multiple tumor-related pathways. Finally, we demonstrated that the knockdown of PCOLCE inhibited glioma development by regulating cell cycle and promoting apoptosis in in vitro experiments. Conclusion PCOLCE promotes glioma progression by regulating multiple tumor-related pathways and immune microenvironment and can be used as a prognostic factor for glioma.","PeriodicalId":14046,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48605626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-03-01DOI: 10.1177/03946320221087922
Farzaneh Koohyanizadeh, Seyed Hamidreza Mortazavi, Farhad Salari, Sara Falahi, Alireza Rezaiemanesh, A. Gorgin Karaji
Background Interleukin-27 (IL-27) is a cytokine composed of two subunits, EBI3 and p28, which is an important mediator in regulating the differentiation of TCD4 + cells and plays an important role in immune-related disorders. This study aimed to elucidate the potential association of single nucleotide polymorphisms (SNPs) of the IL-27p28 gene with serum IL-27 levels and the risk of allergic rhinitis (AR). Materials and methods The study included 130 patients with AR and 130 healthy individuals. To evaluate the association between IL-27p28 gene SNPs (rs153109 and rs181206) and the risk of AR, the Polymerase chain reaction-restriction fragment length polymorphism method was used. Enzyme-linked immunosorbent assay was also used to determine the serum level of IL-27 in patients with AR and healthy individuals. Results Our results did not show a significant relationship between IL-27p28 gene polymorphisms (rs153109 and rs181206) with the risk of AR and serum IL-27 levels. However, our results indicated that the serum level of IL-27 in patients with AR (342 ± 299 pg/mL) was significantly lower than the healthy controls (455 ± 274 pg/mL) (p = 0.02). Conclusion Our findings suggested that IL-27p28 SNPs (rs181206 and rs153109) are not associated with susceptibility to AR, but decreased serum IL-27 levels may be associated with the development of AR.
{"title":"Association between IL-27p28 gene polymorphisms and susceptibility to allergic rhinitis","authors":"Farzaneh Koohyanizadeh, Seyed Hamidreza Mortazavi, Farhad Salari, Sara Falahi, Alireza Rezaiemanesh, A. Gorgin Karaji","doi":"10.1177/03946320221087922","DOIUrl":"https://doi.org/10.1177/03946320221087922","url":null,"abstract":"Background Interleukin-27 (IL-27) is a cytokine composed of two subunits, EBI3 and p28, which is an important mediator in regulating the differentiation of TCD4 + cells and plays an important role in immune-related disorders. This study aimed to elucidate the potential association of single nucleotide polymorphisms (SNPs) of the IL-27p28 gene with serum IL-27 levels and the risk of allergic rhinitis (AR). Materials and methods The study included 130 patients with AR and 130 healthy individuals. To evaluate the association between IL-27p28 gene SNPs (rs153109 and rs181206) and the risk of AR, the Polymerase chain reaction-restriction fragment length polymorphism method was used. Enzyme-linked immunosorbent assay was also used to determine the serum level of IL-27 in patients with AR and healthy individuals. Results Our results did not show a significant relationship between IL-27p28 gene polymorphisms (rs153109 and rs181206) with the risk of AR and serum IL-27 levels. However, our results indicated that the serum level of IL-27 in patients with AR (342 ± 299 pg/mL) was significantly lower than the healthy controls (455 ± 274 pg/mL) (p = 0.02). Conclusion Our findings suggested that IL-27p28 SNPs (rs181206 and rs153109) are not associated with susceptibility to AR, but decreased serum IL-27 levels may be associated with the development of AR.","PeriodicalId":14046,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43484265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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