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Blood, 15 April 2007, Vol. 109, No. 8, pp. 3235-3243. Prepublished online as a Blood First Edition Paper on December 21, 2006; DOI 10.1182/blood-2005-01-015081. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2005-01-015081v1 109/8/3235    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gregory, A. D. Articles by Link, D. C. Search for Related Content PubMed PubMed Citation Articles by Gregory, A. D. Articles by Link, D. C. Related Collections Phagocytes Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Regulation of systemic and local neutrophil responses by G-CSF during pulmonary Pseudomonas aeruginosa infection Alyssa D. Gregory1, Lisa A. Hogue2, Thomas W. Ferkol2, and Daniel C. Link1 1 Department of Medicine, Division of Oncology, and 2 Department of Pediatrics, Washington University School of Medicine, St Louis, MO Granulocyte colony-stimulating factor (G-CSF) regulates the production, maturation, and function of neutrophils. Its expression is often induced during infection, resulting in high concentrations of G-CSF in inflammatory exudates and in the blood, suggesting that it may regulate both local and systemic neutrophil responses. Herein, we characterize the neutrophil response in G-CSFR–/– mice following intratracheal injection with Pseudomonas aeruginosa–laden agarose beads, modeling the pulmonary infection observed in many patients with cystic fibrosis. G-CSFR–/– mice are markedly susceptible to bronchopulmonary P aeruginosa infection, exhibiting decreased survival and bacterial clearance as well as extensive damage to lung tissue. The systemic neutrophil response was mediated primarily by enhanced neutrophil release from the bone marrow rather than increased neutrophil production and was attenuated in G-CSFR–/– mice. Despite normal to increased local production of inflammatory chemokines, neutrophil accumulation into the infected lung of G-CSFR–/– mice was markedly reduced. Moreover, the percentage of apoptotic neutrophils in the lung was elevated, suggesting that G-CSF signals may play an important role in regulating neutrophil survival at the inflammatory site. Collectively, these data provide new evidence that G-CSF signals play important but specific roles in the regulation of the systemic and local neutrophil response following infection. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Sawanobori, S. Ueha, M. Kurachi, T. Shimaoka, J. E. Talmadge, J. Abe, Y. Shono, M. Kitabatake, K. Kakimi, N. Mukaida, et al. Chemokine-mediated rapid turnover of myeloid-derived suppressor cells in tumor-bearing mice Blood, June 15, 2008; 111(12): 5457 - 5466. [Abstract] [Full Text] [PDF] A. M. Wengner, S. C. Pitchford, R. C. Furze, and S. M. Rankin The coordinated action of G-CSF and ELR + CXC chemokines in neutrophil mobilization during acute inflammation Blood, January 1, 2008; 111(1): 42 - 49. [Abstract] [Full Text] [PDF]

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