Background There is considerable controversy around the question as to whether Helicobacter pylori (H. pylori) infection has a protective or causative role in the development of multiple sclerosis (MS). This study evaluated published information to assess the association between H. pylori infection and MS. Methods We conducted a comprehensive systematic review of relevant observational studies in international databases. A random‐effects model was used to calculate pooled odds ratio (OR) and 95% confidence interval (CI). I2 statistic was used to assess the between‐study heterogeneity. Subgroup and meta‐regression analyses were applied to identify the source of heterogeneity. Results In total, 22 studies (25 datasets) were eligible for the meta‐analysis: 17 datasets had prevalence data and eight datasets had data on the mean titer of anti‐H. pylori IgG. The pooled prevalence of H. pylori was 44.1% (908/2606) in the MS patients and 46.1% (1016/2200) in the controls, indicating a non‐significant protective effect of H. pylori on MS (OR, 0.82; 95%CI, 0.58–1.17). In the subgroup analysis, studies that used ELISA yielded a significant protective association (OR, 0.59; 95%CI, 0.46–0.77), while a positive non‐significant association (OR, 1.33; 95%CI, 0.83–2.15) was found from studies that used other serological methods; interestingly, a significant positive association (OR, 6.64; 95%CI, 2.40–13.76) was found from studies that used histological methods to detect H. pylori infection. Conclusions Our findings do not support the hypothesis that H. pylori infection represents a protective factor against the development of MS; however, the results varied depending on the diagnostic method(s). Particularly, a significant positive association was identified when studies introduced results based on histological examination, suggesting that active H. pylori infection might be a risk factor for development of MS. Thus, further studies are needed utilizing accurate diagnostic methods to elucidate the association between active H. pylori infection and MS.
Purpose: Inflammatory bowel disease (IBD) is a life-threatening disorder of the gastrointestinal tract. For the first time, we studied the role of GARP, a crucial regulator of TGF-β synthesis, in Crohn's disease (CD) and ulcerative colitis (UC) patients. We also investigated the upstream regulatory Non-coding RNAs of GARP, namely Lnc-MALAT1 and miR-142-3p. This research sheds light on the mechanisms underlying the development of inflammation in IBD.Methods: A peripheral blood sample was collected from 22 patients with CD, 22 patients with UC, and 22 healthy individuals. PBMCs were isolated, and RNAs were extracted and synthesized into cDNAs. Genes expression was evaluated using the Real-Time PCR method.Results: Our study revealed a decrease in GARP expression in both CD and IBD groups. We also found that the expression of MALAT1 and miR-142-3-p were elevated in CD and IBD groups, contributing to the observed decrease in GARP levels. It also has been discovered that smoking is associated with an increase in MALAT1 expression in all patients.Conclusion: Our research indicates that changes in GARP, MALAT1, and miR-142-3-p levels may be the culprit behind the reduction in TGF-β levels. Moreover, an increase in MALAT1 and miR-142-3-p expression could be responsible for a decrease in GARP levels. These novel biomarkers provide a deeper understanding of the pathways involved in the pathogenesis of IBD and may pave the way for the development of innovative diagnostic or therapeutic approaches.
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