Species-specific immunity to Helicobacter suis

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00027162%3A_____%2F17%3AN0000069" target="_blank" >RIV/00027162:_____/17:N0000069 - isvavai.cz</a>

Výsledek na webu

<a href="http://onlinelibrary.wiley.com/doi/10.1111/hel.12375/full" target="_blank" >http://onlinelibrary.wiley.com/doi/10.1111/hel.12375/full</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1111/hel.12375" target="_blank" >10.1111/hel.12375</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Species-specific immunity to Helicobacter suis

Popis výsledku v původním jazyce

BackgroundHelicobacter (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 MethodsCytokine 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. ResultsDespite 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- and FoxP3 mRNA levels

Název v anglickém jazyce

Species-specific immunity to Helicobacter suis

Popis výsledku anglicky

BackgroundHelicobacter (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 MethodsCytokine 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. ResultsDespite 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- and FoxP3 mRNA levels

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

40301 - Veterinary science

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2017

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Helicobacter

ISSN

1083-4389

e-ISSN

—

Svazek periodika

22

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

e12375

Kód UT WoS článku

000400859900009

EID výsledku v databázi Scopus

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