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The Proinflammatory Role of Guanylate-Binding Protein 5 in Inflammatory Bowel Diseases
NLRP3 inflammasome is implicated in the pathogenesis of inflammatory bowel diseases (IBD). Since guanylate-binding protein 5 (GBP5) induces the NLRP3 inflammasome activity, we aim to investigate the potential role of GBP5 in IBD pathogenesis. The expression of GBP5, NLRP3 inflammasome, and related cytokines and chemokines was examined in two cohorts of IBD patients and healthy controls, by microarray transcriptome analysis and quantitative real-time PCR. Cellular localization of GBP5 in colonic biopsies was examined by immunohistochemistry and immunofluorescence with confocal microscopy. For functional studies, GBP5 was in...
Source: Frontiers in Microbiology - June 2, 2022 Category: Microbiology Source Type: research

The Gut Microbiota-Bile Acids-TGR5 Axis Mediates Eucommia ulmoides Leaf Extract Alleviation of Injury to Colonic Epithelium Integrity
Eucommia ulmoides leaves (EL) are rich in phenolic acids and flavonoids, showing enhancing intestinal health effects. The intestinal microbiota-bile acid axis plays important roles in the occurrence and recovery of inflammatory bowel disease (IBD). However, whether EL extract (ELE) has regulatory effects on the intestinal microbiota, bile acid metabolism, and IBD is still unclear. To fill this gap, 2% dextran sulfate sodium (DSS)-induced mild IBD in a C57BL/6J mouse model that was treated with 200 or 400 mg/kg (intake dose/body weight) ELE was used. Oral ELE supplementation alleviated DSS-induced shortening of colon and co...
Source: Frontiers in Microbiology - August 18, 2021 Category: Microbiology Source Type: research

Notch Signaling Pathway Is Activated by Sulfate Reducing Bacteria
In this study, we tested whether Desulfovibrio, the most dominant SRB genus in the gut, may activate Notch signaling. RAW 264.7 macrophages were infected with Desulfovibrio vulgaris (DSV) and analyzed for the expression of Notch signaling pathway-related proteins. We found that DSV induced protein expression of Notch1 receptor, Notch intracellular domain (NICD) and p21, a downstream Notch target, in a dose-and time-dependent manner. DSV also induced the expression of pro-IL1β, a precursor of IL-1β, and SOCS3, a regulator of cytokine signaling. The gamma secretase inhibitor DAPT or Notch siRNA dampened DSV-induced Notch-r...
Source: Frontiers in cellular and infection microbiology - July 15, 2021 Category: Microbiology Source Type: research

De Novo sphingolipid synthesis is essential for Salmonella -induced autophagy and human beta-defensin 2 expression in intestinal epithelial cells
Conclusions Our results offer mechanistic insights on the role of de novo sphingolipid synthesis in the innate immunity of intestinal epithelial cells to Salmonella infection. The pharmaceuticals enhancing or diet enriched with sphingolipids may induce the dual anti-bacterial mechanisms. The role of de novo sphingolipid synthesis on inflammatory bowel disease is deserved to be further investigated.
Source: Gut Pathogens - February 18, 2016 Category: Microbiology Source Type: research

Differential regulation of interleukin-8 and human beta-defensin 2 in Pseudomonas aeruginosa -infected intestinal epithelial cells
Conclusions: The P. aeruginosa-induced antimicrobial peptide in IECs continuously protect the host against prolonged infection, while modulation of proinflammatory responses prevents the host from the detrimental effects of overwhelming inflammation. Thus, P. aeruginosa-induced innate immunity in IECs represents a host protective mechanism, which may provide new insight into the pathogenesis of inflammatory bowel diseases.
Source: BMC Microbiology - November 30, 2014 Category: Microbiology Authors: Fu-Chen Huang Source Type: research

Review of studies that have used knockout mice to assess normal function of prion protein under immunological or pathophysiological stress
Abstract Deletion of cellular isoform of prion protein (PrPC) increases neuronal predisposition to damage by modulating apoptosis and the negative consequences of oxidative stress. In vivo studies have demonstrated that PrPC‐deficient mice are more prone to seizure, depression, and induction of epilepsy and experience extensive cerebral damage following ischemic challenge or viral infection. In addition, adenovirus‐mediated overexpression of PrPC reduces brain damage in rat models of cerebral ischemia. In experimental autoimmune encephalomyelitis, PrPC‐deficient mice reportedly have a more aggressive disease onset an...
Source: Microbiology and Immunology - July 8, 2014 Category: Microbiology Authors: Takashi Onodera, Akikazu Sakudo, Hirokazu Tsubone, Shigeyoshi Itohara Tags: Review Source Type: research

Studies for normal function of prion protein using knockout mice under the immunological or pathophysiological stress
ABSTRACT Deletion of cellular isoform of prion protein (PrPC) increased neuronal predisposition to damage by modulating to apoptosis, and the negative consequences to oxidative stress. In vivo studies demonstrated that PrPC‐deficient mice were more prone to seizure, depression and epilepsy induction, and exhibited an extent of the cerebral damage following an ischemic challenge or viral infection. Besides, adenovirus‐mediated PrPC over‐expression reduces brain damage in rat model of cerebral ischemia. In experimental autoimmune encephalomyelitis (EAE) PrPC‐deficient mice demonstrated more aggressive disease onset a...
Source: Microbiology and Immunology - May 1, 2014 Category: Microbiology Authors: Takashi Onodera, Akikazu Sakudo, Hirokazu Tsubone, Shigeyoshi Itohara Tags: Review Source Type: research