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Infection and Immunity, January 2005, p. 485-493, Vol. 73, No. 1
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.1.485-493.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

CXCR3 and Its Ligands Participate in the Host Response to Bordetella bronchiseptica Infection of the Mouse Respiratory Tract but Are Not Required for Clearance of Bacteria from the Lung

Daniel P. Widney,1 Yan Hu,1 Amy K. Foreman-Wykert,2 Kim C. Bui,1 Tam T. Nguyen,1 Bao Lu,3 Craig Gerard,3 Jeff F. Miller,2 and Jeffrey B. Smith1*

Departments of Pediatrics,1 Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine, University of California, Los Angeles, California,2 Perlmutter Laboratory, Children's Hospital and Harvard Medical School, Boston, Massachusetts3

Received 15 April 2004/ Returned for modification 18 June 2004/ Accepted 9 September 2004

Intranasal inoculation of mice with Bordetella bronchiseptica produces a transient pneumonia that is cleared over several weeks in a process known to require both neutrophils and lymphocytes. In this study, we evaluated the roles of the chemokines MIG (CXCL9), IP-10 (CXCL10), and I-TAC (CXCL11) and their common receptor, CXCR3. Following bacterial inoculation, message expression of interleukin-1 (IL-1), IL-6, and the neutrophil-attracting chemokines KC, LIX, and MIP-2 was rapidly induced, with maximal expression found at 6 h. In contrast, message expression of gamma interferon, MIG, IP-10, and I-TAC peaked at 2 days. Expression of all of these chemokines and cytokines returned to near baseline by 5 days, despite the persistence of high levels of live bacteria at this time. Induced MIG, IP-10, and I-TAC protein expression was localized in areas of inflammation at 2 to 3 days and was temporally associated with increased levels of CXCR3+ lymphocytes in bronchoalveolar lavage fluid. There was no increase in mortality in mice lacking CXCR3. However, the clearance of bacteria from the lung and trachea was delayed, and the recruitment of lymphocytes and NK cells was slightly decreased, for CXCR3–/– mice relative to CXCR3+/+ mice. We conclude that the CXCR3 receptor-ligand system contributes to pulmonary host defense in B. bronchiseptica infection by recruiting lymphocytes and NK cells into the lung.

* Corresponding author. Mailing address: Division of Neonatology, Department of Pediatrics, David Geffen UCLA School of Medicine, Center for the Health Sciences, 10833 LeConte Ave., Los Angeles, CA 90095. Phone: (310) 206-7632. Fax: (310) 267-0154. E-mail: jbsmith{at}ucla.edu.

Editor: V. J. DiRita

Infection and Immunity, January 2005, p. 485-493, Vol. 73, No. 1
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.1.485-493.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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