Elevated levels of beta-chemokines in bronchoalveolar lavage fluid (BALF) of individuals infected with human T lymphotropic virus type-1 (HTLV-1)

Pulmonary complications are known to develop in HTLV-1 carriers, including T lymphocytic alveolitis, and increased IL-2 receptor alpha (CD25)-bearing T cells have been found in BALF. Several chemokines may contribute to accum ulation of T lymphocytes in the lungs of HTLV-1 carriers. Here, we compared the distribution of T lymphocyte subsets and beta-chemokines, such as macr ophage inflammatory peptide-1 alpha (MIP-1 alpha), regulated on activation normal T expressed and secreted (RANTES), and macrophage chemoattractant pr otein-1 (MCP-1), in BALF and peripheral blood between HTLV-1 carriers and n on-infected healthy normal subjects. Flow cytometric analysis with MoAbs to cell surface antigens was used to identify T lymphocyte subsets in BALF sa mples from HTLV-1 carriers (n = 13) and non-infected healthy controls (n = 10). The levels of different beta-chemokines were estimated by ELISA. High percentages of CD3(+) cells, CD3 expressing HLA-DR antigen and CD3(+)CD25() cells were detected in BALF of HTLV-1 carriers compared with non-infected controls. The concentration of MIP-1 alpha in BALF of patients was signifi cantly higher than in non-infected healthy controls and correlated well wit h the percentage of CD3(+)CD25(+) cells. The level of RANTES in BALF was al so significantly high in HTLV-1 carriers, but did not correlate with the pe rcentage of CD3(+)CD25(+) cells. On the other hand, the level of MCP-1 in B ALF of HTLV-1 carriers was not different from that of controls. Our results suggest a possible interaction between activated T cells bearing CD25 and beta-chemokines, especially MIP-1 alpha, which may contribute to the pulmon ary involvement in HTLV-1 carriers.