Metabolic consequences of Helicobacter pylori infection and eradication

Table 1 Profile of cytokines involved in Helicobacter pylori infection

Cytokine	Cellular origin	Role in gastric mucosa	Implications in metabolic processes
IL-1β	Mucosal and circulating monocytes, mast cells, epidermic and endothelial cells	Proinflammatory molecule, its expression is increased in the infected gastric mucosa. Mast cells stimulated by VacA toxin also produce IL-1β. Certain polymorphisms of IL-1β gene might promote atrophic gastritis and adenocarcinoma[2,9]	IL-1βin vitro induces distruction of pancreatic β cells, in insulin-sensitive organs produces inflammation and insulin resistance. It is increased in type 2 DM and mediates thrombotic complications[3]
IL-6	Monocytes, epithelial and endothelial cells	Innate immune recognition of H. pylori is mediated by TLR4 and induces increased expression of IL-6, IL-8, IL-10,IL-12[2]	IL-6 is increased in diabetes mellitus and in vitro downregulates adiponectin mRNA expression[3]
IL-8	Monocytes, fibroblasts, epithelial and endothelial cells	Secreted upon stimulation by IL-1β and TNF α, Il-8 induces polymorph neutrophil infiltration. H. pylori-infected gastric mucosa and gastric carcinoma cells express increased levels of IL-8. Recruited leucocytes phagocytose opsonized bacteria and produce reactive oxygen and nitrogen species[2,10]	Circulating monocyte IL-8, and TNF α levels are increased in type 2 DM with peripheral vascular disease[3]
IL-10	Th2 cells	Antiinflammatory cytokine but IL-10 gene polymorphism could reduce its production and enhance the risk of gastric cancer[2]	Idem as IL-8
IL-17	Th17 cells	IL-17 regulates the Th2 response to H. pylori and has anti-inflammatory effect[11]	Unknown
TNF α	Macrophages, T cell, natural killer cells	Elevated production TNF α and/or polymorphism of its gene (308 G > A) increase the risk of atrophic gastritis and distal gastric cancer. TNF α inhibits acid secretion[1,2]	Elevated levels in diabetes, obesity and metabolic syndrome alters insulin sensitivity, decreases glucose-transporter 4 and supresses adiponectin, increases the expression of IL-6 and MCP1 genes, promoting atherosclerosis[3]
IFNγ	Th1 cells	INFγ expressed in higher proportion of H. pylori-infected persons than those uninfected, inducing expression of IL-1β, IL-6, IL-8 and TNF α	Serum IF is increased in autoimmune type 1 diabetes. Polymorphism of IFγ is implicated in the pathogenesis of proliferative retinopathy is Type 1 and 2 DM. INFγ is increased in metabolic syndrome[3]

DM: Diabetes mellitus; H. pylori: Helicobacter pylori; IFN: Interferon; MCP-1: Monocyte chemotactic protein-1; TLR: Toll like receptor; IL: Interleukin; TNF: Tumor necrosis factor.