Structural modifications of Helicobacter pylori lipopolysaccharide: An idea for how to live in peace

Figure 2 Helicobacter pylori lipopolysaccharide-mediated immunomodulation. The effector functions of both natural and adaptive immune cells could be downregulated by various lipopolysaccharide (LPS)-dependent mechanisms, making the persistence of Helicobacter pylori (H. pylori) infection possible. These probable mechanisms might include LPS-dependent escape of phagocytosis due to apoptosis of polymorphonuclear cells, downregulation of the cytotoxic activity of natural killer (NK) cells and expansion of NK cells producing regulatory interleukin (IL)-10, expansion of natural killer T cells, inhibition of antigen presentation by mature macrophages, and downregulation of the lymphocyte proliferation indirectly caused by LPS-driven macrophage arrest. Stimulation of B lymphocytes in response to H. pylori LPS may result in the production of anti-Lewis antibodies, which, together with host Lewis antigens, form immune complexes which may induce complement (C)-dependent inflammation. ECM: Extracellular matrix; PRRs: Pathogen recognition receptors; oxLDL: Oxidized low density lipoprotein (LDL).