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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.

Helicobacter pylori Impairs Murine Dendritic Cell Responses to Infection