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Species‐specific immunity to Helicobacter suis

2017; Wiley; Volume: 22; Issue: 3 Linguagem: Inglês

10.1111/hel.12375

1523-5378

Iris Bosschem, Bram Flahou, Kim Van Deun, Stefaan De Koker, Jiřı́ Volf, Annemieke Smet, Richard Ducatelle, Bert Devriendt, Freddy Haesebrouck,

Mycobacterium research and diagnosis

Abstract Background Helicobacter ( H .) suis is mainly associated with pigs, but is also the most prevalent gastric non‐ H. pylori Helicobacter species found in humans. Both H. pylori and H. suis may cause persistent infection of the stomach. Several immune evasion mechanisms have been proposed for H. pylori , which focus to a great extent on its major virulence factors, which are absent in H. suis . The aim of this study was to gain more knowledge on immune evasion by H. suis . Materials and Methods Cytokine expression kinetics were monitored in the stomach of BALB /c mice experimentally infected with H. suis . The cytokine expression profile in the stomach of naturally H. suis ‐infected pigs was also determined. Subsequently, the effect of H. suis on murine and porcine dendritic cell ( DC ) maturation and their ability to elicit T‐cell effector responses was analyzed. Results Despite a Th17/Th2 response in the murine stomach, the inflammatory cell influx was unable to clear H. suis infection. H. suis ‐stimulated murine bone marrow‐derived dendritic cells induced IL ‐17 secretion by CD 4 + cells in vitro . Natural H. suis infection in pigs evoked increased expression levels of IL ‐17 mRNA in the antrum and IL ‐10 mRNA in the fundus. In contrast to mice, H. suis ‐stimulated porcine monocyte‐derived dendritic cells were unable to express MHCII molecules on their cell surface. These semimature DC s induced proliferation of T‐cells, which showed an increased expression of TGF ‐β and FoxP3 mRNA levels. Conclusions Helicobacter suis might evade host immune responses by skewing toward a Treg‐biased response.