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Kohno. Increased expression of collagen-binding heat shock protein 47 in murine bleomycin-induced pneumopathy.

The concentrations of telithromycin, a new ketolide antimicrobial agent, in alveolar macrophages (AMs) and bronchoalveolar epithelial lining fluid (ELF) were determined in order to investigate the transfer of the drug into target tissue, relative to plasma, following multiple oral doses of telithromycin. Twenty-four healthy male Japanese volunteers were randomly allocated to four groups. Each subject was given 600 or 800 mg of telithromycin once daily for 5 days, followed by bronchoalveolar lavage (

SUMMARYPulmonary complications are known to develop in HTLV-1 carriers, including T lymphocytic alveolitis, and increased IL-2 receptor a (CD25)-bearing T cells have been found in BALF. Several chemokines may contribute to accumulation of T lymphocytes in the lungs of HTLV-1 carriers. Here, we compared the distribution of T lymphocyte subsets and b-chemokines, such as macrophage in¯ammatory peptide1a (MIP-1a), regulated on activation normal T expressed and secreted (RANTES), and macrophage chemoattractant protein-1 (MCP-1), in BALF and peripheral blood between HTLV-1 carriers and noninfected healthy normal subjects. Flow cytometric analysis with MoAbs to cell surface antigens was used to identify T lymphocyte subsets in BALF samples from HTLV-1 carriers (n 13) and noninfected healthy controls (n 10). The levels of different b-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-1a in BALF of patients was signi®cantly higher than in non-infected healthy controls and correlated well with the percentage of CD3 CD25 cells. The level of RANTES in BALF was also signi®cantly high in HTLV-1 carriers, but did not correlate with the percentage of CD3 CD25 cells. On the other hand, the level of MCP-1 in BALF of HTLV-1 carriers was not different from that of controls. Our results suggest a possible interaction between activated T cells bearing CD25 and b-chemokines, especially MIP-1a, which may contribute to the pulmonary involvement in HTLV-1 carriers.

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