Role of gut microbiota and Helicobacter pylori in inflammatory bowel disease through immune-mediated synergistic actions

Figure 1 Potential immune mechanisms of Helicobacter pylori on inflammatory bowel disease exacerbation and alleviation. The cytotoxin-associated antigen A gene and NOD-like receptor thermal protein domain associated protein 3 inflammasome activate the Th17/regulatory T (Treg) cell response, stimulating Treg cell, interleukin (IL)-13, and IL-10 expression. IL-13 and IL-10 synergistically promote the macrophage shift to the M2 phenotype and inhibit the M1 phenotype. M2-type macrophages inhibit Toll-like receptor signaling, stimulating CD163 production, and release anti-inflammatory IL-10. However, Helicobacter pylori could increase inflammatory flora, produce endotoxins, modulate the Th17/Treg cell response, contribute to the release of Th17 factors, recruit immune cells, exacerbate inflammation, and worsen inflammatory bowel disease. CagA: Cytotoxin-associated antigen A; H. pylori: Helicobacter pylori; IL: Interleukin; NLRP3: NOD-like receptor thermal protein domain associated protein 3; Treg: Regulatory T; TLR: Toll-like receptor.