Intestinal dysbiosis and probiotic applications in autoimmune diseases

Abstract

In humans, a complex interaction between the host immune system and commensal microbiota is required to maintain gut homeostasis. In this symbiotic relationship, the microbiota provides carbohydrate fermentation and digestion, vitamin synthesis and gut-associated lymphoid tissue development, as well as preventing colonization by pathobionts, whereas the host offers a niche and nutrients for the survival of the microbiota. However, when this mutualistic relationship is compromised and an altered interaction between immune cells and microorganisms occurs, the gut microbiota may cause or contribute to the establishment of infectious diseases and trigger autoimmune diseases. Researchers have made efforts to clarify the role of the microbiota in autoimmune disease development and find new therapeutic approaches to treat immune-mediated diseases. However, the exact mechanisms involved in the dysbiosis and breakdown of the gut epithelial barrier are currently unknown. Here, we provide a general overview of studies describing gut microbiota perturbations in animal models of autoimmune diseases, such as type 1 diabetes, multiple sclerosis, rheumatoid arthritis and systemic lupus erythematosus. Moreover, we include the main studies concerning dysbiosis in humans and a critical discussion of the existing data on the use of probiotics in these autoimmune diseases.

Keywords: autoimmunity; dysbiosis; gut barrier; inflammation; probiotics.

Figure 1

A schematic representation of the interaction between commensal microbiota and the immune system. Under eubiosis, there are microbiota diversity and immune homeostasis in the gut mucosa. Commensal microorganisms instruct dendritic cells to induce IgA‐secreting cell differentiation, and in turn, IgA regulates the composition of the gut microbiota. During dysbiosis, there are decreased diversity in commensal microbiota and deregulated interactions between immune cells and these microorganisms. Some specific bacteria, such as Bacteroides fragilis, induce regulatory T cell differentiation and the secretion of anti‐inflammatory cytokines, whereas segmented filamentous bacteria (SFB) promote T helper type 17 (Th17) cell differentiation and the secretion of pro‐inflammatory cytokines, which play roles in several autoimmune diseases.

Figure 2

A schematic representation of the intestinal dysbiosis in organ‐specific autoimmune diseases in humans.

Figure 3

A schematic representation of intestinal dysbiosis in rheumatic autoimmune diseases in humans.