Recurrent infection progressively disables host protection against intestinal inflammation.
作者： Won Ho Yang , Douglas M. Heithoff , Peter V. Aziz , Markus Sperandio , Victor Nizet
关键词:
摘要: Intestinal inflammation is the central pathological feature of colitis and inflammatory bowel diseases. These syndromes arise from unidentified environmental factors. We found that recurrent nonlethal gastric infections Gram-negative Salmonella enterica Typhimurium (ST), a major source human food poisoning, caused murine intestinal tissue, predominantly colon, which persisted after pathogen clearance irreversibly escalated in severity with repeated infections. ST progressively disabled host mechanism protection by inducing endogenous neuraminidase activity, accelerated molecular aging alkaline phosphatase (IAP). Disease was linked to Toll-like receptor 4 (TLR4)-dependent IAP desialylation accumulation substrate TLR4 ligand, lipopolysaccharide-phosphate. The administration or antiviral inhibitor zanamivir therapeutic maintaining abundance function.
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