The Central Role of the Gut Microbiota in Chronic Inflammatory Diseases

Figure 1

Schematic representation of the pulmonary allergic response induced by gastrointestinal (GI) immune cells and two microbiota-related conditions (a healthy gut microbiota and a reduced gut microbiota following antibiotic treatment). Microbes in the intestines are sampled by Toll-like receptors (TLRs) on DCs either directly in the lumen or in the gut-associated lymphoid tissue (GALT). In the healthy gut microbiota, polymorphonuclear development (PMN) is normal and DCs become regulatory DCs (DCr) that promote development of Tregs and/or Th1 cells and natural killer (NK) cells. These NK cells inhibit Th2 inflammation. Antibiotic treatment kills a large proportion of healthy microbiota, leading to a reduced gut microbiota and an inflammatory environment without DCs, Th1 cells or NK cells. In this environment, an unhealthy microbiota elevates serum immunoglobulin E (IgE) levels, increases circulating basophil populations, and exacerbates basophil-mediated Th2 responses (adapted from Forsythe [110]).