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Clinical and Diagnostic Laboratory Immunology, May 2004, p. 599-607, Vol. 11, No. 3
1071-412X/04/$08.00+0 DOI: 10.1128/CDLI.11.3.599-607.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Department of Veterinary Pathology,1 Veterinary Diagnostic and Production Animal Medicine, College of Veterinary Medicine, Iowa State University, Ames, Iowa 50011-1250,3 Department of Pathology, University of Washington, St. Louis, Missouri,2 Respiratory Diseases of Ruminants Research Unit, Agricultural Research Service, U.S. Department of Agriculture-National Animal Disease Center, Ames, Iowa 500104
Received 21 October 2003/ Returned for modification 26 November 2003/ Accepted 2 January 2004
Defensins and surfactant protein A (SP-A) and SP-D are antimicrobial components of the pulmonary innate immune system. The purpose of this study was to determine the extent to which parainfluenza type 3 virus infection in neonatal lambs alters expression of sheep beta-defensin 1 (SBD-1), SP-A, and SP-D, all of which are constitutively transcribed by respiratory epithelia. Parainfluenza type 3 viral antigen was detected by immunohistochemistry (IHC) in the bronchioles of all infected lambs 3 days postinoculation and at diminished levels 6 days postinoculation, but it was absent 17 days postinoculation. At all times postinoculation, lung homogenates from parainfluenza type 3 virus-inoculated animals had increased SBD-1, SP-A, and SP-D mRNA levels as detected by fluorogenic real-time reverse transcriptase PCR. Protein levels of SP-A in lung homogenates detected by quantitative-competitive enzyme-linked immunosorbent assay and protein antigen of SP-A detected by IHC were not altered. These studies demonstrate that parainfluenza type 3 virus infection results in enhanced expression of constitutively transcribed innate immune factors expressed by respiratory epithelia and that this increased expression occurs concurrently with decreased viral replication.
| Antimicrob. Agents Chemother. | Clin. Microbiol. Rev. | Infect. Immun. |
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