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and Its Receptor CCR1 Control Pulmonary Inflammation and Antiviral Host Defense in Paramyxovirus Infection
*
Department of Pediatrics, State University of New York Upstate Medical University, Syracuse, NY;
Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and
Department of Biological Sciences, University of Warwick, Coventry, United Kingdom
In this work, we explore the responses of specific gene-deleted
mice to infection with the paramyxovirus pneumonia virus of mice (PVM).
We have shown previously that infection of wild type mice with PVM
results in pulmonary neutrophilia and eosinophilia accompanied by local
production of macrophage-inflammatory protein-1
(MIP-1). Here we
examine the role of MIP-1 in the pathogenesis of this disease using
mice deficient in MIP-1 or its receptor, CCR1. The inflammatory
response to PVM in MIP-1-deficient mice was minimal, with 
10–60
neutrophils/ml and no eosinophils detected in bronchoalveolar lavage
fluid. Higher levels of infectious virus were recovered from lung
tissue excised from MIP-1-deficient than from fully competent mice,
suggesting that the inflammatory response limits the rate of virus
replication in vivo. PVM infection of CCR1-deficient mice was also
associated with attenuated inflammation, with enhanced recovery of
infectious virus, and with accelerated mortality. These results suggest
that the MIP-1/CCR1-mediated acute inflammatory response protects
mice by delaying the lethal sequelae of
infection.
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