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Infection and Immunity, November 2004, p. 6221-6229, Vol. 72, No. 11
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.11.6221-6229.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Macrophages from Mice with the Restrictive Lgn1 Allele Exhibit Multifactorial Resistance to Legionella pneumophila

Isabelle Derré1 and Ralph R. Isberg1,2*

Howard Hughes Medical Institute,2 Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts1

Received 19 April 2004/ Returned for modification 19 May 2004/ Accepted 27 May 2004

Although Legionella pneumophila can multiply in diverse cell types from a variety of species, macrophages from most inbred mouse strains are nonpermissive for intracellular replication and allow little or no growth of the bacteria. This phenomenon is likely genetically controlled by the mouse naip5 (birc1e) gene located within the Lgn1 locus. In this study, we have investigated the resistance of C57BL/6J macrophages to L. pneumophila infection by examining the fate of both the bacterium and the infected cells compared to that in macrophages from the permissive A/J strain. Our results indicate that although the trafficking of the L. pneumophila-containing vacuole is partially disrupted in C57BL/6J macrophages, this cannot account for the severity of the defect in intracellular growth observed in this strain. Infected macrophages are lost shortly after infection, and at later times a larger fraction of the C57BL/6J macrophages in which L. pneumophila undergoes replication are apoptotic compared to those derived from A/J mice. Finally, a loss of bacterial counts occurs after the first round of growth. Therefore, the resistance mechanism of C57BL/6J macrophages to L. pneumophila infection appears to be multifactorial, and we discuss how early and late responses result in clearing the infection.

* Corresponding author. Mailing address: Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Harrison Ave., Boston, MA 02111. Phone: (617) 636-3993. Fax: (617) 636-0337. E-mail: ralph.isberg{at}tufts.edu.

Editor: D. L. Burns

Infection and Immunity, November 2004, p. 6221-6229, Vol. 72, No. 11
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.11.6221-6229.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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