Helicobacter pylori (H. pylori) infection has been involved in the pathogenesis of most important gastroduodenal diseases. Matrix metalloproteinases (MMPs) are a large family of zincendopeptidases which play important roles in degradation of extracellular matrix (ECM) and various inflammatory diseases. Therefore, we examined MMP-7 mRNA levels in the gastric mucosa of patients with H. pylori infection and evaluated the effects of virulence factors, such as vacA (vacuolating cytotoxin A) and cagA (cytotoxin-associated gene), in H. pylori-infected patients upon the MMP-7 mRNA mucosal levels. We also determined the correlation between mucosal MMP-7 mRNA levels and the types of disease. Total RNA was extracted from gastric biopsies of 50 H. pylori-infected patients and 50 uninfected individuals. Mucosal MMP-7 mRNA expression level in H. pylori-infected and non-infected gastric biopsies was determined by real-time polymerase chain reaction (PCR). The presences of cagA and vacA virulence factors was evaluated using PCR. MMP-7 expression was significantly higher in biopsies of patients infected with H .pylori compared to uninfected individuals. In addition, mucosal MMP-7 mRNA expression in H. pylori-infected patients significantly associated with the cagA status and the types of disease. Our results suggest that MMP-7 might be involved in the pathogenesis of H. pylori. Peptic ulcer was associated with cag pathogenicity island-dependent MMP-7 upregulation.
The pathogenesis of coronavirus disease 2019 (COVID-19) is not fully elucidated. COVID-19 is due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which causes severe illness and death in some people by causing immune dysregulation and blood T cell depletion. Increased numbers of myeloid-derived suppressor cells (MDSCs) play a diverse role in the pathogenesis of many infections and cancers but their function in COVID-19 remains unclear. To evaluate the function of MDSCs in relation with the severity of COVID-19. 26 PCR-confirmed COVID-19 patients including 12 moderate and 14 severe patients along with 11 healthy age- and sex-matched controls were enrolled. 10 ml whole blood was harvested for cell isolation, immunophenotyping and stimulation. The immunophenotype of MDSCs by flow cytometry and T cells proliferation in the presence of MDSCs was evaluated. Serum TGF-β was assessed by ELISA. High percentages of M-MDSCs in males and of P-MDSCs in female patients were found in severe and moderate affected patients. Isolated MDSCs of COVID-19 patients suppressed the proliferation and intracellular levels of IFN-γ in T cells despite significant suppression of T regulatory cells but up-regulation of precursor regulatory T cells. Serum analysis shows increased levels of TGF-β in severe patients compared to moderate and control subjects (HC) (P = 0.003, P < 0.0001, respectively). The frequency of MDSCs in blood shows higher frequency among both moderate and severe patients and may be considered as a predictive factor for disease severity. MDSCs may suppress T cell proliferation by releasing TGF-β.
Background: Helicobacter pylori has been recognized as the most common pathogen of human gastroduodenal tract and it has been suggested that adhesins, including HopQ and SabA, are associated with the organism's virulence. Objectives: The current study aimed at determining the frequency of hopQI, hopQII, and sabA genes among H. pylori isolates from patients with gastroduodenal disorders in Shahrekord, Iran. Methods: Gastric corpus samples were obtained from 150 symptomatic patients admitted to the endoscopy unit at gastroenterology clinic. After DNA extraction from all corpus samples, H. pylori molecular confirmation and genotyping was performed by the polymerase chain reaction (PCR), using specific primers for glmM, 16SrRNA and hopQ, sabA genes, respectively. Results: The hopQI, hopQII, and sabA genes were found in 74 (49.3%), 59 (39.3%), and 43 (28.7%) cases, respectively. The hopQI gene was detected in 75% of patients with gastric cancer (GC), 42.4% with chronic gastritis (CG), and 57.4% with peptic ulcer disease (PUD). The hopQII among patients with GC, CG, and PUD was also detected in 50%, 38.8%, and 39.3%, respectively. Moreover, sabA was diagnosed in 50% of patients with GC, 29.4% with CG, and 26.2% with PUD. Conclusions: No significant association was observed between hopQI, hopQII, and sabA genes with clinical outcomes.
Helicobacter pylori (H. pylori) is a spiral bacterium that infects the human gastric mucosa. Various clinical aspects of the infection may mirror distinctive forms of cytokine expression. It correlates with immune cell penetration to the gastric mucosa with numerous cytokines production and gastric inflammation. IL-1 and IL-8 directly contribute to H. pylori effected gastritis. IL-32 is a pro-inflammatory cytokine categorized by the training of Immune cell activation, which has a vital role in human immunity. H. pylori virulence and danger factors are critical in gastritis, such as the outer inflammatory protein (OipA) and the cytotoxin associated gene a (cagA). We aimed to study the IL-32 mRNA expression in H. pylori-positive and negative patients as well as its relation with bacterial cagA, oipA, and severity of gastritis. Endoscopic biopsies were taken from the antrum of 60 H. pylori-infected patients and 62 uninfected individuals. Mucosal IL-32 mRNA expression was assessed by real-time PCR. With PCR, the H. pylori virulence factors were evaluated. Showed that the mRNA expression of IL-32 levels was significantly lower in biopsies of H. pylori-uninfected patients compared to positive individuals (P=0.01). A straight communication between virulence factor up, cagA, and heightening in IL-32 mRNA expression (P<0.001) was observed. Furthermore. IL-32 mRNA expression levels were approximately equal in both chronic and active gastritis (P=0.1). IL-32 may have a critical role in different situations like inflammation and the severity of inflammatory changes in the gastric mucosa.
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