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Infection and Immunity, March 2006, p. 1751-1756, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1751-1756.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Cytosolic Phospholipase A₂ Enzymes Are Not Required by Mouse Bone Marrow-Derived Macrophages for the Control of Mycobacterium tuberculosis In Vitro

Department of Microbiology and Immunology, Weill Medical College of Cornell University, and Programs in Immunology and Microbial Pathogenesis and in Molecular Biology, Weill Graduate School of Medical Sciences of Cornell University, New York, New York 10021,¹ Departments of Chemistry and Biochemistry, University of Washington, Seattle, Washington 98195²

Received 7 September 2005/ Returned for modification 14 October 2005/ Accepted 20 December 2005

During the course of infection Mycobacterium tuberculosis predominantly resides within macrophages, where it encounters and is often able to resist the antibacterial mechanisms of the host. In this study, we assessed the role of macrophage phospholipases A₂ (PLA₂s) in defense against M. tuberculosis. Mouse bone marrow-derived macrophages (BMDMs) expressed cPLA₂-IVA, cPLA₂-IVB, iPLA₂-VI, sPLA₂-IIE, and sPLA₂-XIIA. The expression of cPLA₂-IVA was increased in response to M. tuberculosis, gamma interferon, or their combination, and cPLA₂-IVA mediated the release of arachidonic acid, which was stimulated by M. tuberculosis in activated, but not unactivated, macrophages. We confirmed that arachidonic acid is highly mycobactericidal in a concentration- and pH-dependent manner in vitro. However, when M. tuberculosis-infected macrophages were treated with PLA₂ inhibitors, intracellular survival of M. tuberculosis was not affected, even in inducible nitric oxide synthase-deficient macrophages, in which a major bactericidal mechanism is removed. Moreover, intracellular survival of M. tuberculosis was similar in cPLA₂-IVA-deficient and wild-type macrophages. Our results demonstrate that the cytosolic PLA₂s are not required by murine BMDMs to kill M. tuberculosis.

Editor: F. C. Fang

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