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Species-specific immunity to Helicobacter suis

I. Bosschem, B. Flahou, K. Van Deun, S. De Koker, J. Volf, A. Smet, R. Ducatelle, B. Devriendt, F. Haesebrouck,

. 2017 ; 22 (3) : . [pub] 20170126

Jazyk angličtina Země Velká Británie

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc18010836

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 CD4+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 DCs 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.

Citace poskytuje Crossref.org

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