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PLoS One. 2010 May 27;5(5):e10844. doi: 10.1371/journal.pone.0010844.

Helicobacter pylori impairs murine dendritic cell responses to infection.

Author information

  • 1Institute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan, Republic of China.

Abstract

BACKGROUND:

Helicobacter pylori, a human pathogen associated with chronic gastritis, peptic ulcer and gastric malignancies, is generally viewed as an extracellular microorganism. Here, we show that H. pylori replicates in murine bone marrow derived-dendritic cells (BMDCs) within autophagosomes.

METHODOLOGY/PRINCIPAL FINDINGS:

A 10-fold increase of CFU is found between 2 h and 6 h p.i. in H. pylori-infected BMDCs. Autophagy is induced around the bacterium and participates at late time points of infection for the clearance of intracellular H. pylori. As a consequence of infection, LC3, LAMP1 and MHC class II molecules are retained within the H. pylori-containing vacuoles and export of MHC class II molecules to cell surface is blocked. However, formalin-fixed H. pylori still maintain this inhibitory activity in BMDC derived from wild type mice, but not in from either TLR4 or TLR2-deficient mice, suggesting the involvement of H. pylori-LPS in this process. TNF-alpha, IL-6 and IL-10 expression was also modulated upon infection showing a TLR2-specific dependent IL-10 secretion. No IL-12 was detected favoring the hypothesis of a down modulation of DC functions during H. pylori infection. Furthermore, antigen-specific T cells proliferation was also impaired upon infection.

CONCLUSIONS/SIGNIFICANCE:

H. pylori can infect and replicate in BMDCs and thereby affects DC-mediated immune responses. The implication of this new finding is discussed for the biological life cycle of H. pylori in the host.

PMID:
20523725
[PubMed - indexed for MEDLINE]
PMCID:
PMC2877707
Free PMC Article

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