The Journal of Experimental Medicine
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Published online 30 August 2004 doi:10.1084/jem.20040546
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 5, 581-586
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Amphiphysin IIm Is Required for Survival of Chlamydia pneumoniae in Macrophages

Elizabeth S. Gold1, Randi M. Simmons1, Timothy W. Petersen1, Lee Ann Campbell2, Cho-Chou Kuo2, and Alan Aderem1

1 Institute for Systems Biology, Seattle, WA 98103
2 Department of Pathobiology, University of Washington, Seattle, WA 98195

Address correspondence to Alan Aderem, Institute for Systems Biology, 1441 N. 34th St., Seattle, WA 98103. Phone: (206) 732-1203; Fax: (206) 732-1299; email: aderem{at}systemsbiology.org

Macrophages play a critical role in both innate and acquired immunity because of their unique ability to internalize, kill, and degrade bacterial pathogens through the process of phagocytosis. The adaptor protein, amphiphysin IIm, participates in phagocytosis and is transiently associated with early phagosomes. Certain pathogens, including Chlamydia pneumoniae, have evolved mechanisms to subvert macrophage phagosome maturation and, thus, are able to survive within these cells. We report here that, although amphiphysin IIm is usually only transiently associated with the phagosome, it is indefinitely retained on vacuoles containing C. pneumoniae. Under these wild-type conditions, C. pneumoniae do not elicit significant nitric oxide (NO) production and are not killed. Abrogation of amphiphysin IIm function results in C. pneumoniae–induced NO production and in the sterilization of the vacuole. The data suggest that C. pneumoniae retains amphiphysin IIm on the vacuole to survive within the macrophage.

Key Words: innate immunity • bacterial infection • pathogen • phagocytosis • nitric oxide

Abbreviations used in this paper: MOI, multiplicity of infection; NO, nitric oxide.


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