The role of gastrointestinal pathogens in inflammatory bowel disease: a systematic review

Abstract

The inflammatory bowel diseases (IBD), comprising Crohn’s disease (CD) and ulcerative colitis (UC), are chronic, progressive, inflammatory conditions of the gastrointestinal tract. Imbalance in the gut microbial community, or dysbiosis, and the subsequent immune response, represent the critical relationship between genetic susceptibility, microbes, and environment factors, that result in IBD. Gastrointestinal pathogens – a common cause of dysbiosis – have been implicated as an environmental trigger in new onset IBD, as well as flare of existing IBD. In this article, we systematically review clinical data regarding the association between specific gastrointestinal pathogens and IBD. Numerous bacteria, viruses, fungi, and parasites have been implicated in the pathogenesis of IBD, and exacerbations of existing disease. In this article, we will also specifically discuss the less recognized microbes that have an inverse association with IBD, including certain bacterial pathogens, such as Helicobacter pylori, and parasites, such as Trichuris species. Future prospective and experimental studies are required to establish causality and clarify potential mechanisms of enteric pathogens in modifying the risk and course of IBD.

Helicobacter Pylori and Autoimmune Diseases: Involving Multiple Systems

“…In general, gastrointestinal pathogens are thought to be environmental triggers for new IBD and outbreaks of existing ones. But some bacterial pathogens like H. pylori and parasites like trichinella spiralis are negatively correlated with IBD ( 32 , 33 ). Zhao Hui et al ( 34 ) got the conclusion that H. pylori is negatively correlated with IBD, especially CD.…”

Pyrroloquinoline-Quinone Is More Than an Antioxidant: A Vitamin-like Accessory Factor Important in Health and Disease Prevention

“…Bacteria and their products are vital contributors to impairment and permeability of the gut barrier, resulting in an increased influx of bacteria, endotoxin, bacterial DNA, and metabolites into the host circulation. Recent reviews show that microbial dysbiosis and impaired barrier function are associated with gastrointestinal disease [113][114][115], neurodegenerative disease [116][117][118][119], autoimmune disease [120][121][122][123][124][125], and an impaired metabolic status in the host manifested by obesity, insulin resistance and cardiovascular complications [126][127][128][129][130][131][132][133][134][135]. In several animal models [63,64,107,136,137], exposure to PQQ increases mRNA expression levels of tight junction proteins and improves jejunal barrier function, suggesting PQQ may act through the gut to affect tissues in the periphery.…”

cGAS–STING signaling pathway in gastrointestinal inflammatory disease and cancers

“…Moreover, Yersinia DNA was present in 31% (17 of 54 cases) of the specimens from patients with Crohn's disease, while it was not detected in other groups. 70,71 Elevated STING protein levels were observed in the colon from mice infected with Salmonella enterica serovar Typhimurium SL1344 or Citrobacter rodentium, both of which are capable of inducing colitis in mice. 72 However, the causality and potential mechanisms of pathogens in the pathogenesis of IBD, which may involve the detection of pathogen-derived DNA by cGAS-STING signaling pathway, are still unknown.…”