Increased Tumor Necrosis Factor-a (TNF-a) Gene Expression in Parainfluenza Type 1 (Sendai) Virus-Induced Bronchiolar Fibrosis

Increased airway resistance and airway hyperresponsiveness induced in rats by infection with parainfluenza type I (Sendai) virus is associated with bronchiolar fibrosis. To determine whether increased tumor necrosis factor (TNF)-a gene expression is an important regulatory event in virus-induced bronchiolar fibrosis, pulmonary TNF-ea mRNA and protein expression was assessed in rat strains that are susceptible (Brown Norway; BN) and resistant (Fischer 344; F344) to virus-induced bronchiolar fibrosis. Virus-inoculated BN rats had increased TNF-a pulmonary mRNA levels (P < 0.05) and increased numbers of bronchiolar macrophages and fibroblasts expressing TNF-ae protein compared with virus-inoculated F344 rats (P < 0.05). Virus inoculation also induced elevated TNF-a mRNA and protein levels (P < 0.05) in cultured rat alveolar macrophages (NR8383 cells). A 55-kd solu-ble TNF receptor-immunoglobulin G fusion protein (sTNFR-IgG) was used to inhibit TNF-a bioactivity in virus-inoculated BN rats. Treated rats had fewer proliferating bronchiolar fibroblasts, as detected by bromodeoxyuridine incorporation, compared with virus-inoculated control rats (P < 0.05). There was also increased mortality in p55sTNFR-IgG-treated

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