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J Med Microbiol 56 (2007), 305-312; DOI: 10.1099/jmm.0.46913-0
© 2007 Society for General Microbiology
ISSN 1473-5644

Role of Toll-like receptor 2 in recognition of Legionella pneumophila in a murine pneumonia model

Etsu T. Fuse1,2, Kazuhiro Tateda1, Yoshiaki Kikuchi1, Tetsuya Matsumoto3, Fumio Gondaira4, Arata Azuma2, Shoji Kudoh2, Theodore J. Standiford5 and Keizo Yamaguchi1

1 Department of Microbiology and Infectious Diseases, Toho University School of Medicine, Tokyo 143-8540, Japan

2 Fourth Department of Internal Medicine, Nippon Medical School, Tokyo, Japan

3 Department of Microbiology, Tokyo Medical University, Tokyo, Japan

4 Denkaseiken Co. Ltd, Gosenshi, Minami-motomachi 1-2-2, Niigata, Japan

5 Pulmonary and Critical Care Medicine, University of Michigan Medical School, Ann Arbor, MI 48109-0360, USA

Correspondence
Kazuhiro Tateda
kazu{at}med.toho-u.ac.jp

Received 25 August 2006
Accepted 27 October 2006

Legionella pneumophila is an intracellular organism and the major aetiological agent of Legionnaires' disease. Although recent progress has identified Toll-like receptors (TLRs) as receptors for recognition of pathogen-associated molecular patterns in a variety of micro-organisms, understanding the contribution of TLRs to the host response in L. pneumophila infection is still limited. This study examined the roles of TLR2 and TLR4 in murine L. pneumophila pneumonia and an in vitro infection model using bone-marrow-derived macrophages. TLR2-deficient mice, but not TLR4-deficient mice, demonstrated higher lethal sensitivity to pulmonary challenge with L. pneumophila than wild-type mice (P<0.05). Although no differences in pulmonary bacterial burden were observed among the mouse strains examined, lower values of macrophage inflammatory protein-2 (MIP-2), keratinocyte-derived cytokine and interleukin (IL)-6 and higher IL-12 levels were noted in lung homogenates of TLR2-deficient mice compared with the wild-type control and TLR4-deficient mice. Recruitment of inflammatory cells, particularly neutrophils, was severely disturbed in the lungs of TLR2-deficient mice. Reduced MIP-2 production was demonstrated in bone-marrow-derived macrophages from TLR2-deficient mice in response to live L. pneumophila and purified LPS of this strain, but not Escherichia coli LPS. These data highlight the involvement and importance of TLR2 in the pathogenesis of L. pneumophila pneumonia in mice. The results showed that TLR2-mediated recognition of Legionella LPS and subsequent chemokine-dependent cellular recruitment may be a crucial host innate response in L. pneumophila pneumonia.

Abbreviations: BAL, bronchoalveolar lavage; BALF, BAL fluid; BM-M{phi}s, bone-marrow-derived macrophages; EU, endotoxin units; IFN, interferon; IL, interleukin; KC, keratinocyte-derived cytokine; MIP-2, macrophage inflammatory protein-2; TLR, Toll-like receptor.




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