Rewiring host–microbe interactions and barrier function during gastrointestinal inflammation

Abstract

Organismal survival depends on a well-balanced immune system and maintenance of host–microbe mutualism. The fine-tuned relationship between the gut microbiota and host immunity is constantly challenged by opportunistic bacteria testing the integrity of gastrointestinal (GI) barrier defenses. Barrier dysfunction reduces immunological tolerance towards otherwise innocuous microbes; it is a process that may instigate chronic inflammation. Paradoxically, sustained inflammation further diminishes barrier function, enabling bacterial translocation to extra-intestinal tissues. Once translocated, these bacteria stimulate systemic inflammation, thereby compromising organ function. While genetic risk alleles associate with barrier dysfunction, environmental stressors are key triggers of GI inflammation and associated breakdown in immune tolerance towards resident gut microbes. As dietary components dictate substrate availability, they also orchestrate microbiota composition and function, including migratory and pro-inflammatory potential, thus holding the capacity to fuel both GI and extra-intestinal inflammation. Additionally, Western diet consumption may weaken barrier defenses via curbed Paneth cell function and diminished host-defense peptide secretion. This review focuses on intervenable niches of host–microbe interactions and mucosal immunity with the ambition to provide a framework of plausible strategies to improve barrier function and regain tolerance in the inflamed mucosa via nutritional intervention.

High-risk genotypes for type 1 diabetes are associated with the imbalance of gut microbiome and serum metabolites

“…Nevertheless, Eleftherios P Diamandis held that Prevotella copri proliferate in a specific dietary and lifestyle milieu are epiphenomena for a lifestyle ( 41 ). Enrichment of Prevotella copri is predictive for Western individuals responding favorably to a high-fiber, barley-kernel-based diet ( 42 ). These studies ( 41 , 42 ) indicated the influence of diet on the abundance and contrasting effect of Prevotella copri .…”

“…Enrichment of Prevotella copri is predictive for Western individuals responding favorably to a high-fiber, barley-kernel-based diet ( 42 ). These studies ( 41 , 42 ) indicated the influence of diet on the abundance and contrasting effect of Prevotella copri . Further mechanism study of Prevotella copri in relation to T1D is needed.…”

Correlation between altered gut microbiota and elevated inflammation markers in patients with Crohn’s disease

“…The etiology of CD is not fully understood but it is thought to develop as a result of interactions between environmental, microbial, and immune-mediated factors in a genetically susceptible host (1). Gut dysbiosis has been observed in many gastrointestinal diseases (2)(3)(4)(5), including CD. An imbalance of microbiota may be an important indicator of the occurrence and development of CD (6).…”

Vitamin A: a key coordinator of host-microbe interactions in the intestine

“…Therefore, the microbiota modulates the pathogenesis, progression, and treatment of various diseases, and modulating host-microbiota interactions is an emerging therapeutic avenue for disease control and prevention. This complex ecosystem is maintained with the interplay of nutrients, microbiota, and the host that is distinctive along the length of the intestine (1,2,9). The intestinal epithelial cells are located at the vital interface between microbiota/nutrients and the host and play a key role in the host-microbiota-nutrient interplay by functioning as a selective barrier that prevents the entry of harmful molecules while absorbing necessary nutrients (4,10).…”

“…This complex ecosystem is maintained with the interplay of nutrients, microbiota, and the host that is distinctive along the length of the intestine ( 1 , 2 , 9 ). The intestinal epithelial cells are located at the vital interface between microbiota/nutrients and the host and play a key role in the host-microbiota-nutrient interplay by functioning as a selective barrier that prevents the entry of harmful molecules while absorbing necessary nutrients ( 4 , 10 ).…”