Abstract
A previous study showed that virus-resistant F344 rats had higher levels of interferon-γ (IFN-γ)-inducible protein 10 (IP-10) than did virus-susceptible BN rats early after Sendai viral infection. The initial goal of this study was to determine if an early high expression of IP-10 in F344 rats contributes to their resistance to virus-induced airway injury. Infected F344 rats were treated with anti-IP-10 rabbit serum or normal rabbit serum. Results indicated that blocking of IP-10 protein did not significantly change the resistance of F344 rats. However, we observed that neutralization of IP-10 increased IFN-γ protein in bronchoalveolar lavage (BAL) fluid of F344 rats 7 days after inoculation compared with rats that received normal rabbit serum. The pulmonary IFN-γ mRNA abundance remained comparable. This effect was not caused by fluctuation of the viral titer in the lung. This interesting phenomenon suggests that expression of IFN-γ protein can be modulated by treatment with anti-IP-10 antibody at the posttranscriptional or translational level in this model.
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