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Amphiphysin IIm Is Required for Survival of Chlamydia pneumoniae in Macrophages

Gold, Elizabeth S., Simmons, Randi M., Petersen, Timothy W., Campbell, Lee Ann, Kuo, Cho-Chou, Aderem, Alan·2004·The Journal of Experimental Medicine
DOI 10.1084/jem.20040546PMC PMC2212749
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Abstract

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.

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Metadata

Authors
Gold, E. S., Simmons, R. M., Petersen, T. W., Campbell, L. A., Kuo, C.-C., & Aderem, A.
Affiliations
  • 1Institute for Systems Biology, Seattle, WA 98103
  • 2Department of Pathobiology, University of Washington, Seattle, WA 98195
Venue
The Journal of Experimental Medicine
Publisher
Rockefeller University Press
Published
2004-08-30
Volume
200
Issue
5
Pages
581-586
ISSN
  • 1540-9538
  • 0022-1007
DOI
10.1084/jem.20040546
PMC
PMC2212749
Cited by
12
References
0
Language
en

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