Dataset Information

Effects of myeloid differentiation primary response gene 88 (MyD88) activation on Helicobacter infection in vivo and induction of a Th17 response.

ABSTRACT:

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.

SUBMITTER: Obonyo M

PROVIDER: S-EPMC3535435 | biostudies-literature | 2011 Oct

REPOSITORIES: biostudies-literature

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Publications

Effects of myeloid differentiation primary response gene 88 (MyD88) activation on Helicobacter infection in vivo and induction of a Th17 response.

Obonyo Marygorret M Rickman Barry B Guiney Donald G DG

Helicobacter 20111001 5

<h4>Background</h4>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.<h4>Materials and methods</h4>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 ...[more]

PMID: 21923686

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Dataset Information

Effects of myeloid differentiation primary response gene 88 (MyD88) activation on Helicobacter infection in vivo and induction of a Th17 response.

Background

Materials and methods

Results

Conclusion

Publications

Effects of myeloid differentiation primary response gene 88 (MyD88) activation on Helicobacter infection in vivo and induction of a Th17 response.

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