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Infection and Immunity, April 2002, p. 1684-1693, Vol. 70, No. 4
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.4.1684-1693.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

ß-Chemokines Are Induced by Mycobacterium tuberculosis and Inhibit Its Growth

Jussi J. Saukkonen,1* Beth Bazydlo,1 Michael Thomas,1 Robert M. Strieter,2 Joseph Keane,1 and Hardy Kornfeld1

Boston University School of Medicine, Boston, Massachusetts,1 University of California at Los Angeles, Los Angeles, California2

Received 22 June 2001/ Returned for modification 19 September 2001/ Accepted 3 January 2002

Chemokines (CK) are potent leukocyte activators and chemoattractants and aid in granuloma formation, functions critical for the immune response to Mycobacterium tuberculosis. We hypothesized that infection of alveolar macrophages (AM) with different strains of M. tuberculosis elicits distinct profiles of CK, which could be altered by human immunodeficiency virus (HIV) infection. RANTES, macrophage inflammatory protein-1{alpha} (MIP-1{alpha}), and MIP-1ß were the major ß-CK produced in response to M. tuberculosis infection. Virulent M. tuberculosis (H37Rv) induced significantly less MIP-1{alpha} than did the avirulent strain (H37Ra), while MIP-1ß and RANTES production was comparable for both strains. MIP-1{alpha} and MIP-1ß were induced by the membrane, but not cytosolic, fraction of M. tuberculosis. M. tuberculosis-induced CK secretion was partly dependent on tumor necrosis factor alpha (TNF-{alpha}). AM from HIV-infected individuals produced less TNF-{alpha} and MIP-1ß than did normal AM in response to either M. tuberculosis strain. We tested the functional significance of decreased ß-CK secretion by examining the ability of ß-CK to suppress intracellular growth of M. tuberculosis. MIP-1ß and RANTES suppressed intracellular growth of M. tuberculosis two- to threefold, a novel finding. Thus, ß-CK contribute to the innate immune response to M. tuberculosis infection, and their diminution may promote the intracellular survival of M. tuberculosis.

* Corresponding author. Mailing address: Pulmonary Center, Boston University School of Medicine, 80 E. Concord St., R-304, Boston, MA 02118. Phone: (617) 638-6120. Fax: (617) 536-8093. E-mail: jsaukkonen{at}lung.bumc.bu.edu.

Editor: J. T. Barbieri

Infection and Immunity, April 2002, p. 1684-1693, Vol. 70, No. 4
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.4.1684-1693.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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