Suppressive effect of locally produced interleukin-10 on respiratory syncytial virus infection

Abstract

Interleukin (IL)‐10 is known to be a multifunctional cytokine. This study was designed to evaluate the role of IL‐10 during respiratory syncytial virus (RSV) infection using a C57BL/6 transgenic (TG) mouse model in which the expression of murine IL‐10 cDNA was regulated by a human salivary amylase promoter (IL‐10 TG mice). These mice expressed a large amount of IL‐10 in the nasal mucosa and in salivary glands. Viral replication in the respiratory tract after intranasal infection with RSV was suppressed significantly in IL‐10 TG mice compared to non‐transgenic controls. This suppression was IL‐10 specific, because it was prevented by treating mice with neutralizing anti‐IL‐10 antibodies. We also found that IL‐10‐stimulated T cells displayed cytotoxic activity against infected murine nasal epithelial cells. Previous data indicated that IL‐10 induces Fas ligand (L) expression on mouse T cells. Taken together, these data suggest that Fas/Fas L mediated cytotoxicity is involved in the suppression of RSV replication observed in IL‐10 TG mice after intranasal infection.