Gut microbiota as potential orchestrators of irritable bowel syndrome

Abstract

Irritable bowel syndrome (IBS) is a multifactorial functional disorder with no clearly defined etiology or pathophysiology. Modern culture-independent techniques have improved the understanding of the gut microbiota's composition and demonstrated that an altered gut microbiota profile might be found in at least some subgroups of IBS patients. Research on IBS from a microbial perspective is gaining momentum and advancing. This review will therefore highlight potential links between the gut microbiota and IBS by discussing the current knowledge of the gut microbiota; it will also illustrate bacterial-host interactions and how alterations to these interactions could exacerbate, induce or even help alleviate IBS.

Keywords: Dysbiosis; Immunity; Irritable bowel syndrome; Microbiota; Probiotics.

Fig. 1

Factors that might influence the composition of the gut microbiota. Consumption of antibiotics, prebiotics, and probiotics as well as dietary habits have been shown to affect the species of microbiota residing in the gut. These factors will generally dictate which species will become more prevalent. If an expansion of beneficial species occurs through probiotic or prebiotic use, the local pH level is likely to be altered by the beneficial commensals as a means to hamper pathogenic proliferation. Detrimentally, a bout of gastroenteritis in itself alerts the immune system which employs means to remove the offending species. However, the administration of antibiotics in an attempt to solve the problem has potential side effects by depleting levels of commensal microbiota, thus resulting in an opening for nonbeneficial microbiota to establish themselves.

Fig. 2

Illustration of host-microbiota interactions in the gut of irritable bowel syndrome (IBS) patients. Often recorded at lower levels in IBS patients, therapeutic administration of probiotic species such as Bifidobacterium spp. and Lactobacillus spp. have been shown to have positive effects on symptoms of IBS through their anti-inflammatory metabolites (1). Antibiotic use can have potential side effects such as depleting levels of beneficial commensal gut microbiota thus opening niches for nonspecific species to establish themselves (2). Species such as R. gnavus and R. torques are mucin degraders which may breach the mucus barrier allowing for potential pathogenic infiltration (3). Potential inflammation causing species including Streptococcus spp. or Staphylococcus aureus may enter into the epithelial layer and provoke an immune response (4). Diet plays a role in gut microbiota composition since nutrients not absorbed by the host become energy for both beneficial and nonbeneficial gut microbiota (5). Found to be increased in IBS patients, the nonbeneficial gut microbiota Methanogens produce methane which has been shown to slow down gut transit, potentially leading to constipation (6). Beneficial species such as Roseburia spp. produce butyrate, known to help to maintain normal intestinal barrier function through regulation of colon epithelial mucin gene MUC2, a primary component of mucus (7). A potential intestinal dysbiosis of IBS patients may lead to, or be the result of, an altered activity of the mucosal immune system. Although still under debate, increased density of activated mast cells in the mucosa might provoke symptoms (8). Altered macrophage density or function in IBS patients has been suggested leading to a hampered recognition of pathogenic microbiota (9). Possibly, an increased presence or activation of T cells may contribute to symptom generation (10). Also, higher levels of flagellin specific antibodies, as reported in IBS patients, suggests an increased B cell activity (11).