ABSTRACT
We aimed to explore the role of NLRP3 inflammasome in Bifidobacterium longum-regulated visceral hypersensitivity of postinfectious irritable bowel syndrome (PI-IBS). Fifty NIH mice were divided into five groups (n = 10). The visceral sensitivities of PI-2W and PI-8W groups significantly exceeded than those of normal control groups (P < 0.05), which was significantly decreased in PI-B group (P < 0.05). Significantly more IL-18 and IL-1ß were expressed in PI-2W and PI-8W groups than those in normal control groups (P < 0.05), which was significantly decreased in PI-B group (P < 0.05). Bifidobacterium longum may down-regulate IL-18 and IL-1ß expressions by inhibiting NLRP3 inflammasome and thus reduce the visceral hypersensitivity of PI-IBS.
Subject(s)
Bifidobacterium longum/immunology , Inflammasomes/immunology , Irritable Bowel Syndrome/immunology , NLR Family, Pyrin Domain-Containing 3 Protein/immunology , Animals , Intercellular Signaling Peptides and Proteins/immunology , Interleukin-1beta/immunology , MiceABSTRACT
OBJECTIVE: The present study aims to investigate the relationship between genetic polymorphisms in HTR3A and HTR3E and diarrhea predominant irritable bowel syndrome (D-IBS) in a Chinese population. METHODS: We enrolled 500 D-IBS patients and 500 age- and sex-matched healthy control subjects to detect the genotypes in HTR3A and HTR3B gene by using of PCR-RFLP method. RESULTS: There were significant difference between the D-IBS patients and the health control subjects in the distribution of genotype and allele of rs1062613 in HTR3A gene. As regarding rs62625044 in HTR3E gene, we found there was a significant different between the case and the control group in the distribution of GA genotype and A allele in female but not in male. CONCLUSION: The present study suggested that there are associations of D-IBS risk with genetic polymorphisms in HTR3A and HTR3E.
