Inflammatory Bowel Diseases: Host-Microbial-Environmental Interactions in Dysbiosis

Abstract

Crohn’s Disease (CD) and Ulcerative Colitis (UC) are world-wide health problems in which intestinal dysbiosis or adverse functional changes in the microbiome are causative or exacerbating factors. The reduced abundance and diversity of the microbiome may be a result of a lack of exposure to vital commensal microbes or overexposure to competitive pathobionts during early life. Alternatively, many commensal bacteria may not find a suitable intestinal niche or fail to proliferate or function in a protective/competitive manner if they do colonize. Bacteria express a range of factors, such as fimbriae, flagella, and secretory compounds that enable them to attach to the gut, modulate metabolism, and outcompete other species. However, the host also releases factors, such as secretory IgA, antimicrobial factors, hormones, and mucins, which can prevent or regulate bacterial interactions with the gut or disable the bacterium. The delicate balance between these competing host and bacteria factors dictates whether a bacterium can colonize, proliferate or function in the intestine. Impaired functioning of NOD2 in Paneth cells and disrupted colonic mucus production are exacerbating features of CD and UC, respectively, that contribute to dysbiosis. This review evaluates the roles of these and other the host, bacterial and environmental factors in inflammatory bowel diseases.

Extracellular vesicles of Fusobacterium nucleatum compromise intestinal barrier through targeting RIPK1-mediated cell death pathway

“…Also, infection and environmental factors can hyper-activate the intestinal immune and nonimmune system causing damage to the intestinal mucosal barrier. 2 , 3 Moreover, altered intestinal flora and/or disorder of the immune barrier ultimately led to chronic nonspecific inflammation of the intestinal tract. Apoptosis, also known as programmed cell death (PCD), is a vital mechanism that affects intestinal mucosal injury and immune disorders in UC.…”

Bacillus subtilis-Based Probiotic Improves Skeletal Health and Immunity in Broiler Chickens Exposed to Heat Stress

“…It can be further affected by management issues such as rearing conditions (restriction, crowding, heat, cold environments), breeding programs (selected for a special production indicator), and stress-related factors (transportation and weaning) in farm animals [ 16 , 17 , 18 , 19 ]. Impaired gut microbiota (dysbiosis), alterations in the richness and diversity of microbiota, leads to the pathophysiological processes of various diseases in humans and animals [ 20 , 21 , 22 , 23 , 24 ]. The modulation of the gut microbiota by the administration of probiotics, as well as prebiotics and synbiotics, has become a biotherapy strategy for preventing and treating many diseases, from stress-related irritable bowel syndrome to neuropsychiatric disorders [ 25 , 26 , 27 ].…”

Thirdhand cigarette smoke leads to age‐dependent and persistent alterations in the cecal microbiome of mice

“…Tobacco‐related diseases, including cardiovascular disease, Crohn's disease, and cancer, are increasing; however, the role or contribution of THS in these diseases remains largely unknown. Environmental exposures are recognized as important factors that can influence the abundance of specific microbes, which subsequently can act as risk factors for chronic diseases (Colquhoun et al, 2020; Tu et al, 2020). Therefore, the adverse health effects of tobacco smoke including THS may be at least in part mediated by modulating the human gut microbiome.…”

“…Yet studies show that early‐life environmental exposures have persistent effects on microbiome composition and function (Lozupone et al, 2012; Snijders et al, 2016). In recent years, evidence has emerged that exposure to toxic environmental chemicals leads to adverse health effects that are mediated through altering the gut microbiome (Colquhoun et al, 2020; Khan & Wang, 2019; Sbihi et al, 2019; Tsiaoussis et al, 2019; Tu et al, 2020).…”