抄録
Human T-lymphotropic virus type 1 (HTLV-1) is etiologycally associated with not only adult T cell leukemia but also several chronic inflammatory diseases, including bronchopulmonary disorders. To elucidate the pathogenic mechanisms of HTLV-1-associated lung inflammation, we conducted a histopathological and molecular analysis using transgenic mice which bear pX region of this virus. In these mice, accumulations of inflammatory cells, consisting mainly of lymphocytes, were present in peribronchiolar and perivascular areas. The local expression of p 40tax gene was seen in peribronchiolar and, to lesser extent, perivascular area, wich was well consistent with the distribution of lung lesions. Inflammatory cytokines, including IL-1β, TNF-α and IFN-γ, and several chemokines, such as MCP-1, RANTES, MIP-1 α and IP-10, were detected in the lungs of transgenic mice. Moreover, there was a significant correlation between expression of MCP-1 and that of p 40tax and the gene expression of the above chemokines, with the exception of MIP-1α, correlated with the severity of histopathological changes in lungs. Considered collectively, these results suggested that p 40tax synthesis may be involved in the development of lung lesions caused by HTLV-1 through the induction of local production of inflammatory cytokines and chemokines.
