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Institutes of
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Medical Microbiology, Immunology, and Hygiene, and
Clinical Chemistry and Pathobiochemistry, Technical University of Munich, Munich, Germany
Chlamydia pneumoniae is an obligate
intracellular human pathogen causing diseases such as pneumonia,
bronchitis, and pharyngitis. Because of its intracellular replication,
cell-mediated immune responses are needed to mediate successful
defenses of the host. Because dendritic cells play a central role in
linking innate immunity and Ag-specific cell-mediated immune responses
we asked whether dendritic cells are activated upon contact with
C. pneumoniae and whether known Toll like receptors
(TLR) are involved in this process. Here we show that C.
pneumoniae was taken up by bone marrow-derived murine dendritic
cells. Ingested C. pneumoniae appeared to be unable to
develop mature inclusion inside dendritic cells. Furthermore, upon
contact with C. pneumoniae dendritic cells were potently
stimulated because NF-
B was activated and translocated to the
nucleus, cytokines like IL-12p40 and TNF-
were secreted, and
expression of MHC class II molecules, CD40, CD80, and CD86 was
up-regulated. Importantly, secretion of cytokines as well as
translocation of NF-B were dependent on the presence of TLR2 and
independent from TLR4 with the exception of IL-12p40 secretion, which
was attenuated in the absence of either a functional TLR2 or 4. In
conclusion, we show here that recognition of the Gram-negative
bacterium C. pneumoniae depends largely on TLR2 and only
to a minor extent on TLR4.
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