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Published ahead of print on February 10, 2006, doi:10.1165/rcmb.2005-0246OC

Am. J. Respir. Cell Mol. Biol., Volume 34, Number 6, June 2006, 766-774

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Submitted on July 6, 2005
Revised on February 6, 2006

Role of GM-CSF during Gram-negative Lung Infection with Pseudomonas aeruginosa

Megan N Ballinger1, Robert Paine, III2, Carlos H.C. Serezani3, David M Aronoff4, Esther S Choi1, Theodore J Standiford2, Galen B Toews5, and Bethany B Moore2*

1 Immunology Graduate Program, University of Michigan, Ann Arbor, MI, USA, 2 Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, MI, USA, 3 Institute of Biomedical Science IV, University of Sao Paulo, Sao Paulo, Brazil, 4 Department of Internal Medicine, Division of Infectious Diseases, University of Michigan, Ann Arbor, MI, USA, 5 Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, MI, USA; Department of Veterans Affairs Medical Center, VA Medical Center, Ann Arbor, MI, USA

* To whom correspondence should be addressed. E-mail: bmoore{at}umich.edu.

Granulocyte-macrophage-colony-stimulating factor (GM-CSF) stimulates survival, proliferation, differentiation and function of myeloid cells. Recently, GM-CSF has been shown to be important for normal pulmonary homeostasis. We now report that GM-CSF is induced in lung leukocytes during infection with Gram negative bacteria. Therefore, we postulated that deficiencies in GM-CSF would increase susceptibility to Gram-negative infection in vivo. Following an intratracheal (i.t.) inoculum with Pseudomonas aeruginosa, we show GM-CSF-/- mice have decreased survival compared to wild type (WT) mice. GM-CSF-/- mice show increased lung, spleen and blood bacterial CFU. GM-CSF-/- mice are defective in the production of cysteinyl leukotrienes (cys-LTs), prostaglandin E2 (PGE2), macrophage inflammatory protein (MIP-2), and keratinocyte-derived chemokine (KC) in lung leukocytes post-infection. Despite these defects, inflammatory cell recruitment is not diminished at 6 or 24 h post-infection and the functional activity of polymorphonuclear leukocytes (PMNs) from both the lung and peritoneum against P. aeruginosa are enhanced in GM-CSF-/- mice. In contrast, alveolar macrophage (AM) phagocytosis, killing and H2O2 production are defective in GM-CSF-/- mice. Although the absence of GM-CSF had profound effects on AMs, peritoneal macrophages (PM) appear to have normal bactericidal activities in GM-CSF-/- mice. Defects in AM function may be related to diminished levels of interferon (IFN)-{gamma} and tumor necrosis factor (TNF)-{alpha} post-infection. Thus, GM-CSF-/- mice are more susceptible to lung infection with P. aeruginosa as a result of impaired AM function.




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