Gut microbiota and immunity relevance in eubiosis and dysbiosis

Abstract

Human gut is colonized by numerous microorganisms, in which bacteria present the highest proportion of this colonization that live in a symbiotic relationship with the host. This microbial collection is commonly known as the microbiota. The gut microbiota can mediate gut epithelial and immune cells interaction through vitamins synthesis or metabolic products. The microbiota plays a vital role in growth and development of the main components of human's adaptive and innate immune system, while the immune system regulates host-microbe symbiosis. On the other hand, negative alteration in gut microbiota composition or gut dysbiosis, can disturb immune responses. This review highlights the gut microbiota-immune system cross-talk in both eubiosis and dysbiosis.

Keywords: Dysbiosis; Eubiosis; Gut microbiota; Immune system.

Fig. 1

Factors affecting gut microbiota composition: Different factors can influence gut microbial colonization such as mode of delivery and pre-/term-birth, geographical location, diseases, use of drugs, type of food or diet, life style such as exercise, ageing and breast feeding.

Fig. 2

Window of opportunity for gut microbiota modulation: Several factors modulate the gut microbiota in each stage of human life.

Fig. 3

Microbiota-immunity interaction in dysbiosis: Gut dysbiosis can cause immune-mediated disorders in different systems.

Fig. 4

Dysbiosis of gut microbiota and IBD: An increase in the intestinal epithelial cells permeability in IBD during gut dysbiosis induces the production of pro-inflammatory cytokines and activates T cells, macrophages and NK cells. Furthermore, during inflammation adhesion molecules are produced for leucocyte recruitment.

Fig. 5

Association between gut dysbiosis and liver diseases: In gut dysbiosis, bacteria can invade the liver and induce TLR4 by LPS which stimulates different immune responses (proinflammatory cytokines production, adhesion and chemokines expression, etc.) which leads to progression of different diseases (NAFLD).

Fig. 6

Gut dysbiosis can stimulate Rheumatoid arthritis: Gut dysbiosis can induce the production of autoantibodies and inflammatory cytokines that mediate RA.

Fig. 7

Gut microbiota and cardiovascular diseases. TMAO causes atherogenesis by several mechanisms such as platelets hyperreactivity, inflammatory cytokines and reverse cholesterol inhibition.