IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lindell, D. M.
Right arrow Articles by Huffnagle, G. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lindell, D. M.
Right arrow Articles by Huffnagle, G. B.

 Previous Article  |  Next Article 

Infection and Immunity, October 2001, p. 6364-6369, Vol. 69, No. 10
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.10.6364-6369.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Macrophage Inflammatory Protein 1alpha /CCL3 Is Required for Clearance of an Acute Klebsiella pneumoniae Pulmonary Infection

Dennis M. Lindell,1 Theodore J. Standiford,1 Peter Mancuso,2 Zachary J. Leshen,1 and Gary B. Huffnagle1,*

Pulmonary and Critical Care Medicine, The University of Michigan Medical School,1 and Environmental Health Sciences, University of Michigan School of Public Health,2 Ann Arbor, Michigan

Received 25 April 2001/Returned for modification 14 June 2001/Accepted 10 July 2001

The objective of these studies was to determine the role of macrophage inflammatory protein 1alpha /CCL3 in pulmonary host defense during Klebsiella pneumoniae infection. Following intratracheal inoculation, 7-day survival of CCL3-/- mice was less than 10%, compared to 60% for CCL3+/+ mice. Survival of CCR5-/- mice was equivalent to that of controls, indicating that the enhanced susceptibility of CCL3-/- mice to K. pneumoniae is mediated via another CCL3 receptor, presumably CCR1. At day 3, CFU burden in the lungs of CCL3-/- mice was 800-fold higher than in CCL3+/+ mice, demonstrating that CCL3 is critical for control of bacterial growth in the lung. Surprisingly, CCL3-/- mice had no differences in the recruitment of monocytes/macrophages and even showed enhanced neutrophil recruitment at days 1, 2, and 3 postinfection, compared to CCL3+/+ mice. Therefore, the defect in clearance was not due to insufficient recruitment of leukocytes. No significant differences in cytokine levels of monocyte chemoattractant protein 1 (MCP-1), interleukin 12, gamma interferon, or tumor necrosis factor alpha in lung lavages were found between CCL3+/+ and CCL3-/- mice. CCL3-/- alveolar macrophages were found to have significantly lower phagocytic activity toward K. pneumoniae than CCL3+/+ alveolar macrophages. These findings demonstrate that CCL3 production is critical for activation of alveolar macrophages to control the pulmonary growth of the gram-negative bacterium K. pneumoniae.

* Corresponding author. Mailing address: Pulmonary and Critical Care Medicine, 6301 MSRB III, University of Michigan Medical Center, Ann Arbor, MI 48109-0642. Phone: (734) 936-9369. Fax: (734) 764-4556. E-mail: ghuff{at}umich.edu.

Infection and Immunity, October 2001, p. 6364-6369, Vol. 69, No. 10
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.10.6364-6369.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2001 by the American Society for Microbiology. All rights reserved.