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Effects of Myeloid Differentiation Primary Response Gene 88 (MyD88) Activation on Helicobacter Infection In Vivo and Induction of a Th17 Response
Author(s) -
Obonyo Marygorret,
Rickman Barry,
Guiney Donald G.
Publication year - 2011
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1523-5378.2011.00861.x
Subject(s) - in vivo , helicobacter pylori infection , myeloid , gene , helicobacter , immunology , biology , helicobacter pylori , genetics
Background: Helicobacter pylori is a spiral‐shaped Gram‐negative microaerophilic bacterium associated with a number of gastrointestinal disorders, including gastritis, peptic ulcers, and gastric cancer. Several studies have implicated a Th17 response as a key to protective immunity against Helicobacter . Materials and Methods: Wild type (WT) and MyD88‐deficient (MyD88 −/− ) mice in the C57BL/6 background were infected with H. felis for 6 and 25 weeks and colonization density and host response evaluated. Real‐time PCR was used to determine the expression of cytokines and antimicrobial peptides in the gastric tissue of mice. Results: mRNA expression levels of the Th17 cytokines interleukin‐17A (IL‐17A) and IL‐22 were markedly up‐regulated in WT compared with MyD88 −/− mice both at 6 and at 25 weeks in response to infection with H. felis , indicating that induction of Th17 responses depends on MyD88 signaling. Furthermore, reduction in the expression of Th17‐dependent intestinal antimicrobial peptide lipocalin‐2 was linked with increased bacterial burden in the absence of MyD88 signaling. Conclusion: We provide evidence showing that MyD88‐dependent signaling is required for the host to induce a Th17 response for the control of Helicobacter infection.