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. 2020 Jun 9;11:1065. doi: 10.3389/fmicb.2020.01065

FIGURE 1.

FIGURE 1

Macrophages are involved in the interaction between gut microbiota and IBD or Obesity. (A) Under gut homeostasis, bone marrow derived Ly6C+ monocytes are constantly recruited to gut to replenish the intestinal macrophages (CD14– macrophages) which recognize the pathogen through TLR4 receptor and secret anti-inflammatory cytokine IL-10 to promote Treg cell expansion. (B) In IBD, the inflammatory environment lead to gut dysbiosis included increased number of AIEC which can survive and replicate in macrophages, and decreased butyrate bacteria like Ruminococcaceae, Eubacterium, Clostridia, and Firmicutes, which impairs the ability of butyrate exert anti-inflammatory role through inhibiting HDACs/NF-κB (GPR43/41) or promoting IL-10 secretion (GPR109a). Additionally, blood Ly6C+ monocytes are recruited to intestinal to become inflammatory macrophages (CX3CR1+ macrophages) and secrete pro-inflammatory cytokines such as IL-23 and TNF-α to participated in inflammatory response. (C) In Obesity, the alteration of gut microbiota composition caused by HFD-diet lead to an increase of intestinal permeability, therefore LPS enter system circulation (i.e., metabolic endotoxemia). Adipose tissue macrophages are response to LPS activation and transform to M1 phenotype.