RESUMEN
Helicobacter suis colonizes the stomachs of a variety of animals, including humans, and is more likely than other Helicobacter species to induce gastric mucosa-associated lymphoid tissue lymphoma. Obesity is a low-grade chronic inflammatory state in which the induction of a chemokine network contributes to a variety of diseases. However, the effect of obesity on the development of gastric MALT in the presence of H. suis infection remains unclear. Here, we reveal that high-fat-diet-induced obesity upregulates the expression of lymphoid chemokines in the stomach and accelerates the H. suis infection-induced formation of gastric lymphoid follicles, potentially via a mechanism that involves the activation of the nuclear factor kappa B (NF-κB) signaling pathway. These findings provide novel insight into the pathogenesis of obesity-related diseases, especially those induced by Helicobacter infection.
Asunto(s)
Quimiocinas/metabolismo , Dieta Alta en Grasa/efectos adversos , Regulación de la Expresión Génica/efectos de los fármacos , Infecciones por Helicobacter/microbiología , Helicobacter heilmannii , Obesidad/inducido químicamente , Animales , Quimiocinas/genética , Gastritis/microbiología , Infecciones por Helicobacter/patología , Ratones , Estómago/microbiología , Estómago/patologíaRESUMEN
Helicobacter suis has a greater tendency to induce gastric mucosa-associated lymphoid tissue lymphoma compared with other Helicobacter species in humans and animals. Saccharomyces boulardii has been established as an adjunct to H. pylori eradication treatment, but the effect of S. boulardii administration alone on Helicobacter infection remains unclear. Here, we found that S. boulardii administration effectively decreased the bacterial load of H. suis and inhibited the formation of lymphoid follicles in the stomach post-infection. The levels of H. suis-specific immunoglobulin A (IgA) and secretory IgA in the gastric juice and small intestinal secretions and the production of mouse ß-defensin-3 in the small intestinal secretions were significantly increased by S. boulardii administration at 12 weeks after H. suis infection. In addition, feeding with S. boulardii inhibited the expression of inflammatory cytokines and lymphoid follicle formation-related factors after H. suis infection. These results suggested that S. boulardii may be useful for the prevention and treatment of Helicobacter infection-related diseases in humans.