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Am J Physiol Lung Cell Mol Physiol 285: L1263-L1269, 2003. First published August 8, 2003; doi:10.1152/ajplung.00274.2002
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Early high expression of IP-10 in F344 rats resistant to Sendai virus-induced airway injury

Xuezhong Cai and William L. Castleman

Department of Pathobiology, University of Florida, Gainesville, Florida 32610

Submitted 8 August 2002 ; accepted in final form 30 July 2003

Weanling F344 and BN rats differ markedly in their susceptibility to Sendai virus-induced airway injury. Early gene expression that controls their differences in susceptibility remains poorly understood. In this study we combined suppressive subtractive hybridization and cDNA library array hybridization to identify genes differentially expressed in virus-susceptible BN and virus-resistant F344 rats during the first 3 days after inoculation. Differential expression of selected clones was further verified by quantitative RT-PCR. Seven virus-induced gene segments were identified. Of them, interferon-{gamma}-inducible protein 10 (IP-10), Mx1, and guany-late-binding protein-2 mRNA abundance in infected F344 rats was 201.5, 188.2, and 281.7% higher, respectively, than that of infected BN rats at 2 days after inoculation. In situ hybridization indicated that virus-induced IP-10 was expressed mainly in airway epithelial cells of F344 rats. Sendai virus infection can directly induce IP-10 expression in rat tracheal epithelial cells in vitro. IP-10 early high expression might contribute to the resistance to virus-induced airway disease in F344 rats by promoting Th1 responses and increasing antiviral activity.

asthma; parainfluenza type 1; interferon-{gamma}-inducible protein 10; suppressive subtractive hybridization; airway epithelial cells


Address for reprint requests and other correspondence: W. Castleman, Dept. of Pathobiology, Univ. of Florida, PO Box 110880, Gainesville, FL 32610-0880 (E-mail: Castlema{at}ufl.edu).






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