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Infect Immun, March 1998, p. 1121-1126, Vol. 66, No. 3
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Chemokine Production by a Human Alveolar Epithelial Cell Line in Response to Mycobacterium tuberculosis

Yuanguang Lin,1 Ming Zhang,2 and Peter F. Barnes2,*

Division of Infectious Diseases, Department of Medicine, University of Southern California School of Medicine, Los Angeles, California 90033,1 and Center for Pulmonary and Infectious Disease Control, The University of Texas Health Center at Tyler, Tyler, Texas 757102

Received 4 August 1997/Returned for modification 5 September 1997/Accepted 12 December 1997

To investigate the role of chemokines during the initial local response to Mycobacterium tuberculosis in the human lung, we studied chemokine production by the human alveolar epithelial cell line A549 after infection with M. tuberculosis. M. tuberculosis-infected A549 cells produced mRNAs and protein for monocyte chemotactic protein-1 (MCP-1) and interleukin-8 (IL-8) but not mRNAs for macrophage inflammatory protein 1alpha (MIP-1alpha ), MIP-1beta , and RANTES. Chemokine production in response to M. tuberculosis was not dependent on production of tumor necrosis factor alpha, IL-1beta , or IL-6. Two virulent clinical M. tuberculosis isolates, the virulent laboratory strain H37Rv, and the avirulent strain H37Ra elicited production of comparable concentrations of MCP-1 and IL-8, whereas killed M. tuberculosis and three Mycobacterium avium strains did not. The three virulent M. tuberculosis strains grew more rapidly than the avirulent M. tuberculosis strain in the alveolar epithelial cell line, and the three M. avium strains did not grow intracellularly. These findings suggest that intracellular growth is necessary for mycobacteria to elicit production of MCP-1 and IL-8 by alveolar epithelial cells but that virulence and the rate of intracellular growth do not correlate with chemokine production. Alveolar epithelial cells may contribute to the local inflammatory response in human tuberculosis by producing chemokines which attract monocytes, lymphocytes, and polymorphonuclear cells.

* Corresponding author. Mailing address: Center for Pulmonary and Infectious Disease Control, The University of Texas Health Center at Tyler, P.O. Box 2003, Tyler, TX 75710. Phone: (903) 877-5956. Fax: (903) 877-7989. E-mail: pbarnes{at}uthct.edu.




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