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The chemokine macrophage-inflammatory protein-1 alpha and its receptor CCR1 control pulmonary inflammation and antiviral host defense in paramyxovirus infection
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UNSPECIFIED (2000) The chemokine macrophage-inflammatory protein-1 alpha and its receptor CCR1 control pulmonary inflammation and antiviral host defense in paramyxovirus infection. JOURNAL OF IMMUNOLOGY, 165 (5). pp. 2677-2682. ISSN 0022-1767.
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Abstract
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 alpha (MIP-1 alpha). Here we examine the role of MIP-1 alpha in the pathogenesis of this disease using mice deficient in MIP-Io or its receptor, CCR1, The inflammatory response to PVM in MIP-1 alpha -deficient mice was minimal, with similar to 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 alpha -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 alpha /CCR1-mediated acute inflammatory response protects mice by delaying the lethal sequelae of infection.
| Item Type: | Journal Article | ||||
|---|---|---|---|---|---|
| Subjects: | Q Science > QR Microbiology > QR180 Immunology | ||||
| Journal or Publication Title: | JOURNAL OF IMMUNOLOGY | ||||
| Publisher: | AMER ASSOC IMMUNOLOGISTS | ||||
| ISSN: | 0022-1767 | ||||
| Official Date: | 1 September 2000 | ||||
| Dates: |
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| Volume: | 165 | ||||
| Number: | 5 | ||||
| Number of Pages: | 6 | ||||
| Page Range: | pp. 2677-2682 | ||||
| Publication Status: | Published |
Data sourced from Thomson Reuters' Web of Knowledge
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