Epithelial-microbial diplomacy: escalating border tensions drive inflammation in inflammatory bowel disease

Abstract

Inflammatory bowel diseases (IBD) are chronic conditions of the gastrointestinal tract-the main site of host-microbial interaction in the body. Development of IBD is not due to a single event but rather is a multifactorial process where a patient’s genetic background, behavioral habits, and environmental exposures contribute to disease pathogenesis. IBD patients exhibit alterations to gut bacterial populations “dysbiosis” due to the inflammatory microenvironment, however whether this alteration of the gut microbiota precedes inflammation has not been confirmed. Emerging evidence has highlighted the important role of gut microbes in developing measured immune responses and modulating other host responses such as metabolism. Much of the work on the gut microbiota has been correlative and there is an increasing need to understand the intimate relationship between host and microbe. In this review, we highlight how commensal and pathogenic bacteria interact with host intestinal epithelial cells and explore how altered microenvironments impact these connections.

Melatonin in the colon modulates intestinal microbiota in response to stress and sleep deprivation

“…Additionally, it is inversely associated with intestinal inflammation and protect the epithelium from colitis by secreting extracellular vesicles. [36][37][38] In our study, Lactobacillus was reduced in the water stress group but was increased in the melatonin-treated group, consistent with results of melatonin administration in weaning stress mice. 39 In the melatonin treated group, B. massiliensis and Erysipelotrichaceae showed decreases in abundance.…”

Role of the microbiota in ileitis of a mouse model of inflammatory bowel disease—Glutathione peroxide isoenzymes 1 and 2‐double knockout mice on a C57BL background

“…Wild‐type, transgenic, and gene knockout (KO) rodent models of inflammatory bowel disease (IBD) most often demonstrate dependence on gut microbiota (Kiesler, Fuss, & Strober, 2015; Mizoguchi & Mizoguchi, 2010; Peloquin & Nguyen, 2013). This is in line with discoveries of bacterial alterations in IBD in humans (King & McCole, 2019; Sartor & Wu, 2017; Zuo & Ng, 2018). The question persists whether altered microbiomes cause IBD or are a result of IBD.…”

Glutathione S‐transferase theta 1 protects against colitis through goblet cell differentiation via interleukin‐22

“…Mucin produced by goblet cells is the first-line host defense to pathogens or ROS and functions as a reservoir and regulator of AMPs. 28,29 Indeed, decreased mucin level is also characteristic of IBDs, 17,30 and the Muc2 mutation induces spontaneous colitis in mice. 31 Our analysis of mucin-related gene expression and staining of mucin demonstrated that GSTT1 mediates mucin production and goblet cell differentiation induced by cytokines (eg, TNF-α and IL-22) and ROS (eg, H 2 O 2 ).…”