			Home About us Contact

Mucosal Expression (mucosal + expression)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

TLR4 monoclonal antibody blockade suppresses dextran-sulfate-sodium-induced colitis in mice

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 1 2010
Yi Liu
Abstract Background and Aim:, Ulcerative colitis (UC) refers to a kind of inflammatory bowel disease, of which the accurate pathogenesis is not yet well understood. Recently, the toll-like receptor 4 (TLR4) and the TLR4 signaling pathway have been proved as playing an important role in the pathogenesis of UC. The objective of this study was to evaluate the effect of TLR4 monoclonal antibody on dextran-sulfate-sodium-induced colitis in a mouse model. Methods:, We evaluated the effects of the TLR4 monoclonal antibody (TLR4mAb) on the development of dextran-sulfate-sodium-(DSS)-induced colitis. Tissue samples were evaluated by the disease activity index and histopathological score. Meanwhile, the mucosal mRNA expression of cytokines, tumor necrosis factor-,, interferon-, and interleukin-1, were analyzed by semiquantitative reverse transcription polymerase chain reaction. The mucosal protein P38-MAPK, c-jun and c-fos expressions of the TLR4-P38MAPK pathway were analyzed using Western blot. Results:, After the treatment with TLR4mAb against DSS-induced colitis, the bodyweight was significantly increased and both disease activity index and histopathological score were decreased significantly. Furthermore, the mucosal expression of messenger RNA of tumor necrosis factor-,, interferon-, and interleukin-1, were observed to be 8,15-fold more than the baseline, whereas the mucosal expressions of P38MAPK and c-jun were found to be decreased. Conclusion:, Blocking TLR4 by TLR4mAb can prevent the development of DSS-induced colitis through the TLR4-P38MAPK-c-jun pathway. [source]

Peroxiredoxin I protects gastric mucosa from oxidative injury induced by H. pylori infection

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2008
Daisuke Sato
Abstract Background and Aim:, Helicobacter pylori (H. pylori) infection enhances the production of reactive oxygen species and peroxynitrite, thereby resulting in oxidative tissue damage. In this study, we examined the role of peroxiredoxin I (Prx I), a stress-induced antioxidant enzyme, in protecting gastric mucosa from H. pylori -induced gastric mucosal injury. Methods:, Wild type (Prx I+/+) and Prx I-deficient type (Prx I,/,) mice were maintained for 2 to 12 months with or without infection of H. pylori, Sydney strain-1. Gastric mucosal expression of Prx I was assessed by immunoblot analysis and immunohistochemistry. The degree of gastritis was evaluated by the updated Sydney system and by mucosal levels of inflammatory cytokines (MIP-2, IL-1,, and TNF-,). Oxidative DNA injury and apoptosis were analyzed by mucosal level of 8-hydroxy-2,-deoxyguanosine, and the number of apoptotic cells stained with a single-stranded DNA antibody, respectively. Results:,H. pylori infection upregulated gastric mucosal Prx I expression in the Prx I+/+ but not the Prx I,/, mice. H. pylori infection also induced more severe gastritis and a more prominent increase in MIP level, more marked oxidative DNA injury, and apoptosis in the Prx I,/, than the Prx I+/+ mice. In the absence of H. pylori infection, no changes were demonstrated in gastric mucosa in either the Prx I+/+ or the Prx I,/, mice. Conclusion:, These data suggest that H. pylori infection upregulates gastric mucosal Prx I expression, and further, that Prx I plays an important role in gastric mucosal protection against oxidative injury induced by H. pylori infection. [source]

Low-dose aspirin reduces the gene expression of gastrokine-1 in the antral mucosa of healthy subjects

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2008
G. MARTIN
Summary Background, Gastrokine 1 (GKN1), one of the most abundant transcripts in normal stomach, is down-regulated by Helicobacter pylori infection. Aspirin (ASA), which is often used for secondary prevention of cardiovascular events, can damage gastric-duodenal mucosa within 1 or 2 h of ingestion. Aim, To study the gastric mucosal expression of GKN1 during acute low-dose ASA consumption. Methods, Ten H. pylori -negative human volunteers took 100 mg ASA per day for 1 week, and underwent multiple upper GI endoscopies. GKN1 expression was analysed in antral and corpus mucosa by quantitative reverse-transcriptase polymerase chain reaction, western blot and immunohistochemistry (IHC). Gastric mucosal damage was detected endoscopically and histologically. Results, Gastrokine 1 was similarly expressed in both antral and corpus mucosa. The use of low-dose ASA led to a significant decrease (3.07 a.u. vs. 0.23 a.u., P < 0.001) in antrum at day 7, while GKN1 transcript levels in corpus mucosa were slightly elevated (twofold, P < 0.005). Western blot and IHC confirmed these changes at the protein level. Furthermore, IHC revealed a vesicular staining pattern in the cytoplasm for GKN1 that was confirmed by transfected human gastric adenocarcinoma cell line expressing GKN1. Conclusion, Our data demonstrated that low-dose ASA downregulates GKN1 expression specifically in antral mucosa. [source]