Pub Date : 2023-08-08DOI: 10.1177/1721727x231194595
HeHe Sun, Hongmin Wang, Chenhui Gao, Li Tai, Yueyao Yang, Hongliang Dong, Xiaoming Gao
Rheumatoid arthritis is an autoimmune disease characterized by synovial inflammation-driven cartilage and bone destruction, a process mainly mediated by osteoclasts. In recent years M2-like macrophages have been found to play an important role in the pathological process of RA by mediating pro-inflammatory effects, but their roles in the bone destruction of autoimmune arthritis have not been reported. In this study we identified that an abundant cell population of CD45+CD11b+Gr-1-F4/80+CD206+ cells, which were normally classified as M2-like macrophages, was present in synovium of collagen-induced arthritis (CIA) mice, and these cells had the potential to differentiate into osteoclasts. These M2-like macrophages sorted from CIA synovium highly expressed RANK and could be activated by RANKL and M-CSF to acquire osteoclast markers and bone resorption function both in vitro and in vivo. Furthermore, in vitro differentiated M2 macrophages from both CIA mouse bone marrow and RA patient peripheral blood mononuclear cells were also able to differentiate into osteoclasts, confirming the general osteoclastogenesis capability of M2 subtype macrophages. All these results suggest that synovial F4/80+CD206+ M2-like macrophages in RA may be novel osteoclast precursors and contribute significantly to bone erosive changes seen in RA. Our studies provided new directions and targets for the diagnosis and treatment of rheumatoid arthritis.
{"title":"F4/80+CD206+ M2-like macrophages contribute to bone erosion in collagen-induced arthritis by differentiating into osteoclasts","authors":"HeHe Sun, Hongmin Wang, Chenhui Gao, Li Tai, Yueyao Yang, Hongliang Dong, Xiaoming Gao","doi":"10.1177/1721727x231194595","DOIUrl":"https://doi.org/10.1177/1721727x231194595","url":null,"abstract":"Rheumatoid arthritis is an autoimmune disease characterized by synovial inflammation-driven cartilage and bone destruction, a process mainly mediated by osteoclasts. In recent years M2-like macrophages have been found to play an important role in the pathological process of RA by mediating pro-inflammatory effects, but their roles in the bone destruction of autoimmune arthritis have not been reported. In this study we identified that an abundant cell population of CD45+CD11b+Gr-1-F4/80+CD206+ cells, which were normally classified as M2-like macrophages, was present in synovium of collagen-induced arthritis (CIA) mice, and these cells had the potential to differentiate into osteoclasts. These M2-like macrophages sorted from CIA synovium highly expressed RANK and could be activated by RANKL and M-CSF to acquire osteoclast markers and bone resorption function both in vitro and in vivo. Furthermore, in vitro differentiated M2 macrophages from both CIA mouse bone marrow and RA patient peripheral blood mononuclear cells were also able to differentiate into osteoclasts, confirming the general osteoclastogenesis capability of M2 subtype macrophages. All these results suggest that synovial F4/80+CD206+ M2-like macrophages in RA may be novel osteoclast precursors and contribute significantly to bone erosive changes seen in RA. Our studies provided new directions and targets for the diagnosis and treatment of rheumatoid arthritis.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2023-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47107093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-08-07DOI: 10.1177/1721727x231192289
Daoxu Qu, Peiwen Feng, Xinjie Zhang, Mingjie Zhou
This study aimed to evaluate the cardioprotective effects and mechanism of scutellarin (Scu) on heart ischaemia/reperfusion (I/R) injury by using an isolated Langendorff rat heart model. Myocardial function was evaluated via measurements of cardiac haemodynamic parameters. Myocardial infarct size was macroscopically estimated by using TTC staining. The release of creatine kinase (CK) and lactate dehydrogenase (LDH) was used to evaluate cardiac injury. GSH/GSSG, SOD, and MDA were determined as being indicators of oxidative stress. CRP, IL-6, and TNF-α were also analysed to assess inflammation in the heart tissues. Cardiomyocyte apoptosis was quantified by using a TUNEL kit. PPARγ, Nrf2, and NF-κB were assayed via Western blotting. The results indicated that I/R induced significant cardiac dysfunction, myocardial infarct, and apoptosis, as well as decreasing the GSH/GSSG ratio, SOD activity, Nrf2 protein expression, and PPARγ protein expression, but increased levels of TNF-α, MDA, CRP, IL-6, and NF-κB. These data suggest that Scu attenuates cardiac I/R.
{"title":"Effects of scutellarin on acute myocardial ischemia/reperfusion injury in isolated rat heart","authors":"Daoxu Qu, Peiwen Feng, Xinjie Zhang, Mingjie Zhou","doi":"10.1177/1721727x231192289","DOIUrl":"https://doi.org/10.1177/1721727x231192289","url":null,"abstract":"This study aimed to evaluate the cardioprotective effects and mechanism of scutellarin (Scu) on heart ischaemia/reperfusion (I/R) injury by using an isolated Langendorff rat heart model. Myocardial function was evaluated via measurements of cardiac haemodynamic parameters. Myocardial infarct size was macroscopically estimated by using TTC staining. The release of creatine kinase (CK) and lactate dehydrogenase (LDH) was used to evaluate cardiac injury. GSH/GSSG, SOD, and MDA were determined as being indicators of oxidative stress. CRP, IL-6, and TNF-α were also analysed to assess inflammation in the heart tissues. Cardiomyocyte apoptosis was quantified by using a TUNEL kit. PPARγ, Nrf2, and NF-κB were assayed via Western blotting. The results indicated that I/R induced significant cardiac dysfunction, myocardial infarct, and apoptosis, as well as decreasing the GSH/GSSG ratio, SOD activity, Nrf2 protein expression, and PPARγ protein expression, but increased levels of TNF-α, MDA, CRP, IL-6, and NF-κB. These data suggest that Scu attenuates cardiac I/R.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2023-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45041827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-08-04DOI: 10.1177/1721727x231194240
A. Blagov, A. Zhuravlev, V. Sukhorukov, Mikhail Aleksandrovich Popov, A. Grechko, A. N. Orekhov
Systemic lupus erythematosus (SLE) manifests itself in the form of damage to various organs as a result of an autoimmune reaction to the organism's own molecules. Understanding the processes leading to the activation of the autoimmune response, as well as identifying potential autoantigens and their role in the pathogenesis of SIE, is an important task for understanding the mechanisms underlying the pathogenesis of SLE. Here we describe a model of SLE pathogenesis in which the induction of an autoimmune response is based on mitochondrial antigens. In addition to options for initiating an autoimmune response involving mitochondrial components, the model describes the role of pathways and immune cells of these pathways of adaptive immunity in SLE, as well as factors leading to the development of chronic inflammation in SLE. The creation of such models is important for a better understanding of the pathogenesis of SLE, as well as the identification of new therapeutic targets for this disease.
{"title":"Model of the systemic lupus erythematosus pathogenesis based on an autoimmune response to mitochondrial components","authors":"A. Blagov, A. Zhuravlev, V. Sukhorukov, Mikhail Aleksandrovich Popov, A. Grechko, A. N. Orekhov","doi":"10.1177/1721727x231194240","DOIUrl":"https://doi.org/10.1177/1721727x231194240","url":null,"abstract":"Systemic lupus erythematosus (SLE) manifests itself in the form of damage to various organs as a result of an autoimmune reaction to the organism's own molecules. Understanding the processes leading to the activation of the autoimmune response, as well as identifying potential autoantigens and their role in the pathogenesis of SIE, is an important task for understanding the mechanisms underlying the pathogenesis of SLE. Here we describe a model of SLE pathogenesis in which the induction of an autoimmune response is based on mitochondrial antigens. In addition to options for initiating an autoimmune response involving mitochondrial components, the model describes the role of pathways and immune cells of these pathways of adaptive immunity in SLE, as well as factors leading to the development of chronic inflammation in SLE. The creation of such models is important for a better understanding of the pathogenesis of SLE, as well as the identification of new therapeutic targets for this disease.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2023-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44583337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose: To explore the application of intelligent nursing (IN) based on the Internet of Things (IoT) in children with pneumonia and sepsis treated with human gamma globulin (HGG). Methods: A total of 200 children with pneumonia combined with sepsis who attended the First People’s Hospital of Shangqiu from January 1, 2020 to February 13, 2022 were consecutively collected. Children were randomly divided into IN group and routine nursing (RN) group, with 100 children in each group. All children received standard anti-infection treatment along with intravenous HGG. In IN group, IN measures based on the IoT cloud computing platform monitored the treatment process of children with HGG throughout the whole process, while children in the RN group only received RN measures. Information on both groups was collected from the medical records, such as gender, age, duration of hospitalization, fever, antibiotic use, serological indicators, pulmonary function indicators, immune function indicators and adverse effects of HGG. Multi-factorial logistic regression was performed to access the correlation between IN and the duration of hospitalization and a range of other factors studied above. Results: After adjusting for numerous confounding factors, multifactorial logistic regression revealed that the application of IN was associated with a shorter duration of hospitalization ( p = .030) and lower white blood cell (WBC) and creatinine (Cr) levels in post-treatment children ( p = .003, p = .010). It was also associated with higher levels of forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and peak expiratory flow (PEV) after treatment ( p = .014, p = .001, p = .002) and higher levels of immune CD4+/CD8+ ratio after treatment ( p = .001) and reduced symptoms of vomiting among the adverse effects ( p = .047). Conclusion: The IoT cloud-based IN model significantly improved the efficacy of HGG in the treatment of pneumonia sepsis in children and reduce occurrence of some adverse reactions.
目的:探讨基于物联网(IoT)的智能护理(IN)在接受人γ球蛋白(HGG)治疗的肺炎脓毒症患儿中的应用。方法:连续收集2020年1月1日至2022年2月13日在商丘市第一人民医院就诊的肺炎合并脓毒症患儿200例。将患儿随机分为IN组和常规护理组，每组100例。所有儿童均接受标准抗感染治疗并静脉注射HGG。In组基于IoT云计算平台的In措施全程监控HGG患儿的治疗过程，而RN组患儿仅接受RN措施。从病历中收集两组患者的信息，如性别、年龄、住院时间、发热、抗生素使用、血清学指标、肺功能指标、免疫功能指标和HGG的不良反应。我们采用多因素logistic回归来获得IN与住院时间以及上述研究的一系列其他因素之间的相关性。结果:在对众多混杂因素进行校正后，多因素logistic回归显示，使用IN与治疗后儿童住院时间缩短(p = 0.030)和白细胞(WBC)和肌酐(Cr)水平降低相关(p = 0.003, p = 0.010)。治疗后的一秒钟用力呼气量(FEV1)、用力肺活量(FVC)和呼气峰流量(PEV)水平升高(p = 0.014, p = 0.001, p = 0.002)，治疗后免疫CD4+/CD8+比值升高(p = 0.001)，不良反应中呕吐症状减轻(p = 0.047)。结论:基于IoT云的IN模型可显著提高HGG治疗儿童肺炎脓毒症的疗效，减少部分不良反应的发生。
{"title":"Application of intelligent nursing based on cloud computing of internet of things in children with pneumonia and sepsis treated with human gamma globulin","authors":"Aihua Qin, Yuling Liu, Changming Shao, Hongyan Dong","doi":"10.1177/1721727x231194144","DOIUrl":"https://doi.org/10.1177/1721727x231194144","url":null,"abstract":"Purpose: To explore the application of intelligent nursing (IN) based on the Internet of Things (IoT) in children with pneumonia and sepsis treated with human gamma globulin (HGG). Methods: A total of 200 children with pneumonia combined with sepsis who attended the First People’s Hospital of Shangqiu from January 1, 2020 to February 13, 2022 were consecutively collected. Children were randomly divided into IN group and routine nursing (RN) group, with 100 children in each group. All children received standard anti-infection treatment along with intravenous HGG. In IN group, IN measures based on the IoT cloud computing platform monitored the treatment process of children with HGG throughout the whole process, while children in the RN group only received RN measures. Information on both groups was collected from the medical records, such as gender, age, duration of hospitalization, fever, antibiotic use, serological indicators, pulmonary function indicators, immune function indicators and adverse effects of HGG. Multi-factorial logistic regression was performed to access the correlation between IN and the duration of hospitalization and a range of other factors studied above. Results: After adjusting for numerous confounding factors, multifactorial logistic regression revealed that the application of IN was associated with a shorter duration of hospitalization ( p = .030) and lower white blood cell (WBC) and creatinine (Cr) levels in post-treatment children ( p = .003, p = .010). It was also associated with higher levels of forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and peak expiratory flow (PEV) after treatment ( p = .014, p = .001, p = .002) and higher levels of immune CD4+/CD8+ ratio after treatment ( p = .001) and reduced symptoms of vomiting among the adverse effects ( p = .047). Conclusion: The IoT cloud-based IN model significantly improved the efficacy of HGG in the treatment of pneumonia sepsis in children and reduce occurrence of some adverse reactions.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2023-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47398023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-07-27DOI: 10.1177/1721727x231192833
Rui Zhang, Jing Peng, Zhimin Ran, Ranning Xu, Zhiqiang Jin, Y. Sun, Lei Lang, Jing Tao
To evaluate the value of single or combined detection of procalcitonin (PCT), interleukin-6 (IL-6), serum amyloid A (SAA) and c-reactive protein (CRP) in the differential diagnosis of simple and strangulated intestinal obstruction. This retrospectively study collected 61 patients with intestinal obstruction. The patients were classified into the group of simple or strangulated intestinal obstruction according to operation. The age, sex, basic diseases, lesion sites and inflammatory indicators such as PCT, IL-6, SAA and CRP in two groups were collected and analyzed. The Students’ T-test and the Mann-Whitney U test were used to analyze normally and non-normally distributed data, respectively. The categorical variable was analyzed by the chi-square test. The receiver-operating characteristic (ROC) curve and the area under the curve (AUC) were used to predict the differential diagnostic value of single and combined detection of the above clinical inflammatory indicators. The serum levels of PCT, IL-6, SAA and CRP of the strangulated group were significantly higher than those of the simple group ( p < .05). The areas under the ROC curve (AUC) were 0.907 for PCT, 0.712 for IL-6, 0.723 for SAA and 0.681 for CRP. With the cutoff values of PCT (0.24 ng/L), IL-6 (19.55 pg/L), SAA (282.50 mg/L) and CRP (63.00 mg/L), the sensitivity and specificity were 86.40% and 87.20% for PCT, 68.20% and 76.90% for IL-6, 59.10% and 87.20% for SAA, 63.60% and 87.20% for CRP, respectively. And the sensitivity and specificity were 86.40% and 89.70% for combined model. The differences between PCT and the combined model are tiny and neither clinically nor statistically significant. For discriminating strangulated intestinal obstruction from simple intestinal obstruction, PCT alone may be the preferred approach due to its simplicity.
{"title":"Diagnostic value of procalcitonin, interleukin-6, serum amyloid A and C-reactive protein in simple and strangulated intestinal obstruction","authors":"Rui Zhang, Jing Peng, Zhimin Ran, Ranning Xu, Zhiqiang Jin, Y. Sun, Lei Lang, Jing Tao","doi":"10.1177/1721727x231192833","DOIUrl":"https://doi.org/10.1177/1721727x231192833","url":null,"abstract":"To evaluate the value of single or combined detection of procalcitonin (PCT), interleukin-6 (IL-6), serum amyloid A (SAA) and c-reactive protein (CRP) in the differential diagnosis of simple and strangulated intestinal obstruction. This retrospectively study collected 61 patients with intestinal obstruction. The patients were classified into the group of simple or strangulated intestinal obstruction according to operation. The age, sex, basic diseases, lesion sites and inflammatory indicators such as PCT, IL-6, SAA and CRP in two groups were collected and analyzed. The Students’ T-test and the Mann-Whitney U test were used to analyze normally and non-normally distributed data, respectively. The categorical variable was analyzed by the chi-square test. The receiver-operating characteristic (ROC) curve and the area under the curve (AUC) were used to predict the differential diagnostic value of single and combined detection of the above clinical inflammatory indicators. The serum levels of PCT, IL-6, SAA and CRP of the strangulated group were significantly higher than those of the simple group ( p < .05). The areas under the ROC curve (AUC) were 0.907 for PCT, 0.712 for IL-6, 0.723 for SAA and 0.681 for CRP. With the cutoff values of PCT (0.24 ng/L), IL-6 (19.55 pg/L), SAA (282.50 mg/L) and CRP (63.00 mg/L), the sensitivity and specificity were 86.40% and 87.20% for PCT, 68.20% and 76.90% for IL-6, 59.10% and 87.20% for SAA, 63.60% and 87.20% for CRP, respectively. And the sensitivity and specificity were 86.40% and 89.70% for combined model. The differences between PCT and the combined model are tiny and neither clinically nor statistically significant. For discriminating strangulated intestinal obstruction from simple intestinal obstruction, PCT alone may be the preferred approach due to its simplicity.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2023-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48045062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-07-17DOI: 10.1177/1721727x231188546
Qihua Dang, Xingqi Wu, Jing-jing Xu, Shun-min Zhang, M. He
Objective: Clear cell renal cell carcinoma (ccRCC) accounts for 80% of all renal cancers and has a poor prognosis. Studies have found that the abnormal expression of claudins (CLNDs) can influence the functions of tight junctions (TJs) and plays an important role in the occurrence, development, and metastasis of malignant tumours in a variety of epithelial malignant tumours. However, the roles of the different CLNDs in ccRCC are poorly understood. Methods: Used the GEPIA, UALCAN, HPA, Kaplan-Meier Plotter, cBioPortal, String-DB, GeneMANIA, Metascape, and TIMER databases to collect data. Results: The expression levels of CLDN7, 8, 10, 11, 14, 16, and 19 were significantly reduced and promoters were hypermethylated in ccRCC-affected tissues. ccRCC patients with low expression levels are associated highly with the clinical cancer stages, tumour grades, and poor overall survival. Protein interaction and enrichment analysis showed the differential expressions of CLDNs were primarily associated with epithelial cell differentiation and regulation of cell adhesion. Moreover, differential expressions of CLDNs were significantly correlated with the infiltration of diverse immune cells, including six types of CD4+ T cells, macrophages, neutrophils, B cells, CD8+ T cells, and dendritic cells in ccRCC. Conclusion: They are expected to serve as biomarkers for predicting the prognosis of ccRCC patients.
{"title":"Comprehensive analysis of the expression and prognosis value of claudin family members in clear cell renal cell carcinoma","authors":"Qihua Dang, Xingqi Wu, Jing-jing Xu, Shun-min Zhang, M. He","doi":"10.1177/1721727x231188546","DOIUrl":"https://doi.org/10.1177/1721727x231188546","url":null,"abstract":"Objective: Clear cell renal cell carcinoma (ccRCC) accounts for 80% of all renal cancers and has a poor prognosis. Studies have found that the abnormal expression of claudins (CLNDs) can influence the functions of tight junctions (TJs) and plays an important role in the occurrence, development, and metastasis of malignant tumours in a variety of epithelial malignant tumours. However, the roles of the different CLNDs in ccRCC are poorly understood. Methods: Used the GEPIA, UALCAN, HPA, Kaplan-Meier Plotter, cBioPortal, String-DB, GeneMANIA, Metascape, and TIMER databases to collect data. Results: The expression levels of CLDN7, 8, 10, 11, 14, 16, and 19 were significantly reduced and promoters were hypermethylated in ccRCC-affected tissues. ccRCC patients with low expression levels are associated highly with the clinical cancer stages, tumour grades, and poor overall survival. Protein interaction and enrichment analysis showed the differential expressions of CLDNs were primarily associated with epithelial cell differentiation and regulation of cell adhesion. Moreover, differential expressions of CLDNs were significantly correlated with the infiltration of diverse immune cells, including six types of CD4+ T cells, macrophages, neutrophils, B cells, CD8+ T cells, and dendritic cells in ccRCC. Conclusion: They are expected to serve as biomarkers for predicting the prognosis of ccRCC patients.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2023-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48121528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-07-14DOI: 10.1177/1721727x231190246
S. Bilgin, Ahmet Yekta Tüzün
The two most common types of inflammatory bowel disease (IBD) are ulcerative colitis (UC) and Crohn’s disease (CD). Although these diseases mainly affect the intestinal system, they can also affect other systems, especially the vascular system. The objective of this study is to evaluate ocular microvascular and structural changes in IBD. A total of 42 patients with IBD (22 UC and 20 CD) followed in the gastroenterology clinic and 42 healthy controls matched for gender and age were enrolled in the study. All participants underwent optical coherence tomography angiography. Macular vessel density, central retinal, and choroidal thicknesses were measured. No significant differences were observed between IBD patients and control subjects as regards superficial vascular plexus density, deep vascular plexus density, and choriocapillaris vascular density, retinal and choroidal thickness in the macular area ( p > .05). Although not statistically significant, vascular density generally increased. On the other hand, retinal and choroidal thickness were decreased. It could be said that there is a reactive increase in retinal vascular density and a decrease in retinal and choroidal thickness as a result of atherosclerotic changes in IBD.
{"title":"Evaluation of vascular density and structural changes in inflammatory bowel diseases","authors":"S. Bilgin, Ahmet Yekta Tüzün","doi":"10.1177/1721727x231190246","DOIUrl":"https://doi.org/10.1177/1721727x231190246","url":null,"abstract":"The two most common types of inflammatory bowel disease (IBD) are ulcerative colitis (UC) and Crohn’s disease (CD). Although these diseases mainly affect the intestinal system, they can also affect other systems, especially the vascular system. The objective of this study is to evaluate ocular microvascular and structural changes in IBD. A total of 42 patients with IBD (22 UC and 20 CD) followed in the gastroenterology clinic and 42 healthy controls matched for gender and age were enrolled in the study. All participants underwent optical coherence tomography angiography. Macular vessel density, central retinal, and choroidal thicknesses were measured. No significant differences were observed between IBD patients and control subjects as regards superficial vascular plexus density, deep vascular plexus density, and choriocapillaris vascular density, retinal and choroidal thickness in the macular area ( p > .05). Although not statistically significant, vascular density generally increased. On the other hand, retinal and choroidal thickness were decreased. It could be said that there is a reactive increase in retinal vascular density and a decrease in retinal and choroidal thickness as a result of atherosclerotic changes in IBD.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2023-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47938828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-29DOI: 10.1177/1721727x231183670
B. Zhou, Xueping Yue, S. Liang, S. Shang, L. Xiang, K. Zhou, Linfeng Li
Objective: To evaluate the association between IL-25, IL-33 and AD more generally. Methods: Databases, including PubMed, Web of Science, EMBASE, Scopus, CNKI and Sinomed were searched. Based on the criteria, publications were collected. The evaluation of study quality was through Newcastle-Ottawa Scale (NOS). Fixed or random effect model was selected according to the between-study heterogeneity to evaluate the association. The analysis procedure and the construction plots were using Review Manager 5.3 software. Results: Six studies were included. A total of 282 subjects were included from four studies to analyze the association between IL-25 and AD. The level of IL-25 was significantly elevated in AD patients, comparing with the control subjects (SMD = 0.89, 95% CI: 0.64, 1.14, p < 0.05). For IL-33, a total of 247 subjects were included from two studies, and the level of IL-33 was also significantly elevated in AD patients comparing to the control subjects (SMD = 0.49, 95% CI: 0.19, 0.80, p < 0.05). Conclusions: The serum levels of IL-25, IL-33 are elevated in AD patients of this study. The IL-25 and IL-33 are significantly associated with the risk of AD. Further studies with larger samples, in multiple countries and focused on different age groups are need.
目的：更全面地评价IL-25、IL-33与AD的关系。方法：检索PubMed、Web of Science、EMBASE、Scopus、CNKI、Sinomed等数据库。根据这些标准，收集了出版物。学习质量评价采用纽卡斯尔-渥太华量表（NOS）。根据研究之间的异质性选择固定或随机效应模型来评估相关性。分析程序和施工图使用Review Manager 5.3软件。结果：纳入6项研究。从四项研究中共纳入282名受试者，以分析IL-25与AD之间的关系。与对照受试者相比，AD患者的IL-25水平显著升高（SMD=0.89，95%CI:0.64，1.14，p<0.05）。就IL-33而言，两项研究共纳入247名受试人，与对照组相比，AD患者的IL-33水平也显著升高（SMD=0.49，95%CI:0.19，0.80，p<0.05）。结论：本研究的AD患者血清IL-25、IL-33水平升高。IL-25和IL-33与AD的风险显著相关。需要在多个国家和不同年龄组进行更大样本的进一步研究。
{"title":"Association between IL-25, IL-33 and atopic dermatitis: A systematic review and meta-analysis","authors":"B. Zhou, Xueping Yue, S. Liang, S. Shang, L. Xiang, K. Zhou, Linfeng Li","doi":"10.1177/1721727x231183670","DOIUrl":"https://doi.org/10.1177/1721727x231183670","url":null,"abstract":"Objective: To evaluate the association between IL-25, IL-33 and AD more generally. Methods: Databases, including PubMed, Web of Science, EMBASE, Scopus, CNKI and Sinomed were searched. Based on the criteria, publications were collected. The evaluation of study quality was through Newcastle-Ottawa Scale (NOS). Fixed or random effect model was selected according to the between-study heterogeneity to evaluate the association. The analysis procedure and the construction plots were using Review Manager 5.3 software. Results: Six studies were included. A total of 282 subjects were included from four studies to analyze the association between IL-25 and AD. The level of IL-25 was significantly elevated in AD patients, comparing with the control subjects (SMD = 0.89, 95% CI: 0.64, 1.14, p < 0.05). For IL-33, a total of 247 subjects were included from two studies, and the level of IL-33 was also significantly elevated in AD patients comparing to the control subjects (SMD = 0.49, 95% CI: 0.19, 0.80, p < 0.05). Conclusions: The serum levels of IL-25, IL-33 are elevated in AD patients of this study. The IL-25 and IL-33 are significantly associated with the risk of AD. Further studies with larger samples, in multiple countries and focused on different age groups are need.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2023-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45119832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-29DOI: 10.1177/1721727x231182622
Jianyu Feng, Yandong Liu, Chunnan Zhang, Menglin Ji, Cuiyun Li
Phytic acid (PYT) also known as inositol hexakisphosphate or inositol polyphosphate has shown a broad range of biological effects including anti-inflammatory, antioxidant, and anticancer effects in several preclinical studies. This study aimed to investigate the effects of PYT in vitro on HCT116 and HT-29 cell lines and to analyse the intricate mechanism of NF-κB-β-catenin signalling pathways. Both cell lines were treated with PYT, and analysed for cell viability, apoptosis, progression of cell cycle, and DNA fragmentation. Gene and protein expression analysis was performed to assess the molecular mechanism. PYT suppressed the proliferation of colorectal cancer cell lines in a dose- and time-dependent manner with an estimated IC50 value of 2.96 and 3.35 mm, respectively. PYT caused cell cycle arrest at the G2/M phase in both CRC cell lines and induced mitochondrial intrinsic apoptosis via activation of caspase-9 and caspase-3 cascade. PYT suppressed the expression of pro-inflammatory markers especially COX-2 and iNOS, and IL-lβ, IL-6, and IL-10. Analysing the mechanism behind the effects of PYT showed that it suppressed the levels of NF-κB and β-catenin and inhibited the levels of cyclin Dl and c-Myc (its downstream targets) and COX-2. The results collectively indicate the potent anti-inflammatory and anti-proliferative effects of PYT in CRC cell lines that were mediated by downregulating the β-catenin and NF-κB signalling pathways. Results advocate that natural supplementation of PYT can be an effective preventive approach in controlling cancer of colorectal region.
{"title":"Phytic acid regulates proliferation of colorectal cancer cells by downregulating NF-kB and β-catenin signalling","authors":"Jianyu Feng, Yandong Liu, Chunnan Zhang, Menglin Ji, Cuiyun Li","doi":"10.1177/1721727x231182622","DOIUrl":"https://doi.org/10.1177/1721727x231182622","url":null,"abstract":"Phytic acid (PYT) also known as inositol hexakisphosphate or inositol polyphosphate has shown a broad range of biological effects including anti-inflammatory, antioxidant, and anticancer effects in several preclinical studies. This study aimed to investigate the effects of PYT in vitro on HCT116 and HT-29 cell lines and to analyse the intricate mechanism of NF-κB-β-catenin signalling pathways. Both cell lines were treated with PYT, and analysed for cell viability, apoptosis, progression of cell cycle, and DNA fragmentation. Gene and protein expression analysis was performed to assess the molecular mechanism. PYT suppressed the proliferation of colorectal cancer cell lines in a dose- and time-dependent manner with an estimated IC50 value of 2.96 and 3.35 mm, respectively. PYT caused cell cycle arrest at the G2/M phase in both CRC cell lines and induced mitochondrial intrinsic apoptosis via activation of caspase-9 and caspase-3 cascade. PYT suppressed the expression of pro-inflammatory markers especially COX-2 and iNOS, and IL-lβ, IL-6, and IL-10. Analysing the mechanism behind the effects of PYT showed that it suppressed the levels of NF-κB and β-catenin and inhibited the levels of cyclin Dl and c-Myc (its downstream targets) and COX-2. The results collectively indicate the potent anti-inflammatory and anti-proliferative effects of PYT in CRC cell lines that were mediated by downregulating the β-catenin and NF-κB signalling pathways. Results advocate that natural supplementation of PYT can be an effective preventive approach in controlling cancer of colorectal region.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2023-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42272411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objectives: Epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells (RTECs) is a pathogenic factor for renal interstitial fibrosis (RIF). Interleukin-33 (IL-33) is related to the occurrence and development of RIF, but the underlying mechanism remains unclear. Here, we investigated whether IL-33 mediates the EMT of RTECs by activating the NF-κB/Twist1 signalling pathway. Methods: In vivo, the RIF animal model induced by unilateral ureteral obstruction (UUO) was established. The effects of exogenous IL-33 and anti-IL-33 antibodies were evaluated. In vitro, the EMT of RTECs was induced by IL-33. The inhibition of the nuclear factor kappa-B (NF-κB) by the pyrrolidine dithiocarbamate (PDTC) and the knockdown of the suppression of tumorigenicity 2 (ST2) by small interference RNA were used to observe whether IL-33 mediates the EMT of RTECs through the NF-κB/Twist1 signaling pathway. Results: In vivo, exogenous IL-33 significantly aggravated UUO-induced pathological damage and collagen deposition, down-regulated E-cadherin expression, and up-regulated α-smooth muscle actin and Vimentin expressions. Moreover, exogenous IL-33 increased the levels of phospho-IκB-α (p-IκB-α) and phospho-NF-κB p65 (p-NF-κB p65), NF-κB p65 nuclear translocation, and Twist1 nuclear expression. However, these effects were reversed by the anti-IL-33 antibody. In vitro , the increases in the levels of p-IκB-α, p-NF-κB p65, NF-κB p65 nuclear translocation, and Twist1 nuclear expression induced by IL-33 were inhibited by the knockdown of PDTC or ST2. IL-33-mediated EMT of RTECs was also significantly reversed. However, NF-κB inhibitor PDTC had no significant effect on ST2 expression. Conclusions: The IL-33/ST2 axis may up-regulate the expression of Twist1 through the NF-κB signalling pathway, thereby inducing the EMT of RTECs and leading to RIF.
{"title":"Interleukin-33 promotes the epithelial-mesenchymal transition of renal tubular epithelial cells via the NF-κB/Twist1 signalling pathway","authors":"Ziyu Zhang, Wenqiang Gu, Zepeng Li, Xiao Chen, Weixing Xu, Xianwei Li","doi":"10.1177/1721727x231186877","DOIUrl":"https://doi.org/10.1177/1721727x231186877","url":null,"abstract":"Objectives: Epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells (RTECs) is a pathogenic factor for renal interstitial fibrosis (RIF). Interleukin-33 (IL-33) is related to the occurrence and development of RIF, but the underlying mechanism remains unclear. Here, we investigated whether IL-33 mediates the EMT of RTECs by activating the NF-κB/Twist1 signalling pathway. Methods: In vivo, the RIF animal model induced by unilateral ureteral obstruction (UUO) was established. The effects of exogenous IL-33 and anti-IL-33 antibodies were evaluated. In vitro, the EMT of RTECs was induced by IL-33. The inhibition of the nuclear factor kappa-B (NF-κB) by the pyrrolidine dithiocarbamate (PDTC) and the knockdown of the suppression of tumorigenicity 2 (ST2) by small interference RNA were used to observe whether IL-33 mediates the EMT of RTECs through the NF-κB/Twist1 signaling pathway. Results: In vivo, exogenous IL-33 significantly aggravated UUO-induced pathological damage and collagen deposition, down-regulated E-cadherin expression, and up-regulated α-smooth muscle actin and Vimentin expressions. Moreover, exogenous IL-33 increased the levels of phospho-IκB-α (p-IκB-α) and phospho-NF-κB p65 (p-NF-κB p65), NF-κB p65 nuclear translocation, and Twist1 nuclear expression. However, these effects were reversed by the anti-IL-33 antibody. In vitro , the increases in the levels of p-IκB-α, p-NF-κB p65, NF-κB p65 nuclear translocation, and Twist1 nuclear expression induced by IL-33 were inhibited by the knockdown of PDTC or ST2. IL-33-mediated EMT of RTECs was also significantly reversed. However, NF-κB inhibitor PDTC had no significant effect on ST2 expression. Conclusions: The IL-33/ST2 axis may up-regulate the expression of Twist1 through the NF-κB signalling pathway, thereby inducing the EMT of RTECs and leading to RIF.","PeriodicalId":55162,"journal":{"name":"European Journal of Inflammation","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2023-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44109633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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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