The Interaction of Gut Microbiota with Host Immune Responses: Friends or Foes

Abstract

Human gut is associated with trillions of bacteria, ten times higher than the number of the cells in the mammalian body. So the microbiota can be considered as a separate organ. Their presence seems inert in the case of commensals or has beneficial roles in symbionts. In certain circumstances when the gut barrier is disrupted, the gut microbiota can generate immune responses detrimental to the human host. Besides that, irregular distribution of commensal bacteria is linked with the metabolic disorder, obesity, inflammatory bowel disease and cancer [1]. The underlying mechanism of host-gut microbe interactions are still not clear and better knowledge will help to prevent diseases and in the generation of targeted therapy. The impact of the gut microbiota is not only limited to the mucosal surface but it also regulates distant organ sites by promoting innate immune cell development by hematopoiesis. Disruption of the gut microbiota or dysbiosis can lead to gastric ulcers, nonalcoholic fatty liver disease, obesity, metabolic syndromes and hypertension; inflammatory bowel disease, colon cancer, mood and behavioral changes through hormone signaling. The gut microbiota also controls the colonization of pathogenic microbes. The role of gut microbiota and host interactions in metabolic and cardiovascular diseases will be highlighted in this editorial. The link between gut flora and the development of obesity is well established. In genetically obese mice or in obese human volunteers, a significant alteration in Bacteroidetes and Firmicutes was observed compared to lean controls [2]. The microbial production of short-chain fatty acids (SCFA), trimethylamine, acetaldehyde and inflammatory mediators has been shown to significantly impact the metabolic health of the host through pathways that influence satiety, gut permeability and immune function. N-butyrate generated from SCFA regulates leptin production in adipocytes and also controls antiinflammatory responses by reducing cytokine-chemokine release by immune cells. So, targeting butyrate and butyrate producing gut-bacteria can be a new way of restoring host immune function and regulation of energy metabolism [3]. Cardiovascular disease (CVD) is widely recognized as an inflammatory disease. Chronic inflammation is an independent risk factor for atherosclerosis by promoting plaque formation and inducing endothelial dysfunction. Coronary heart disease (CHD) occurs significantly more frequently in patients with inflammatory bowel disease (IBD). However, there is an ongoing debate whether heart disease is linked to viral or bacterial infection. A 13-year study period with 272 adults with nontyphoidal Salmonella NTS bacteremia showed 35% of the patients have extra-intestinal focal infections; 15% developed mycotic aneurysm exclusively after age 45 years, and the rates of mycotic aneurysm (bacterial infection of the arterial wall) increased with the age of patients with NTS bacteremia.