Immune response modulation in inflammatory bowel diseases by Helicobacter pylori infection

Figure 1 Mechanisms of Helicobacter pylori cytotoxin-associated antigen A+ on favorable prognosis of inflammatory bowel diseases. The presence of the cytotoxin-associated antigen A gene at the Cag pathogenicity island induces the modulation of T helper 17/Treg immunological response (1), which reduces levels of interleukin (IL)-17F, IL-17A, and IL-21 and increases the expression of IL-13, IL-10, and Treg (2). These two factors are synergists in the conversion process of the M1 to M2 macrophage lineage (3). Then, M2 macrophages suppress signaling mediated by toll-like receptors (4) and activate metabolic pathways mediated by basic leucine zipper transcription factor ATF-like 2, increasing CD163, a macrophage/monocyte scavenger receptor (5). Finally, the levels of IL-10 expression also increase (6), leading to anti-inflammatory effects (7) and, therefore, to a better prognosis on inflammatory bowel diseases. H. pylori: Helicobacter pylori; IL: Interleukin; TLR: Toll-like receptor; IBD: Inflammatory bowel disease; CagA: Cytotoxin-associated antigen A; Treg: Regulatory T.