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Infection and Immunity, September 1999, p. 4912-4916, Vol. 67, No. 9
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Role of Complement Receptors in Uptake of Mycobacterium avium by Macrophages In Vivo: Evidence from Studies Using CD18-Deficient Mice

Luiz E. Bermudez,1,* Joseph Goodman,2 and Mary Petrofsky1

Kuzell Institute for Arthritis and Infectious Diseases, California Pacific Medical Center Research Institute, San Francisco, California 94115,1 and Laboratory of Electron Microscopy, Department of Pediatrics, University of California, San Francisco, San Francisco, California 941432

Received 22 March 1999/Returned for modification 10 May 1999/Accepted 2 June 1999

Mycobacterium avium is an intracellular pathogen that has been shown to invade macrophages by using complement receptors in vitro, but mycobacteria released from one cell can enter a second macrophage by using receptors different from complement receptors. Infection of CD18 (beta 2 integrin) knockout mice and the C57 BL/6 control mice led to comparable levels of tissue infection at 1 day, 2 days, 1 week, and 3 weeks following administration of bacteria. A histopathological study revealed similar granulomatous lesions in the two mouse strains, with comparable numbers of organisms. In addition, transmission electron microscopy of spleen tissues from both strains of mice showed bacteria inside macrophages. Our in vivo findings support the hypothesis that M. avium in the host is likely to use receptors other than CR3 and CR4 receptors to enter macrophages with increased efficiency.

* Corresponding author. Mailing address: Kuzell Institute, 2200 Webster St., Suite 305, San Francisco, CA 94115. Phone: (415) 561-1734. Fax: (415) 441-8548. E-mail: luizb{at}cooper.cpmc.org.

Infection and Immunity, September 1999, p. 4912-4916, Vol. 67, No. 9
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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Copyright © 1999 by the American Society for Microbiology. All rights reserved.