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Marked inhibition of the intracellular multiplication of Legionella pneumophila in monocytes isolated from carriers of human T lymphotropic virus type I
Author(s) -
Funai Noriko,
Shimamoto Yoshinori,
Watanabe Masayuki,
Yoshida Shinlchi,
Kohashi Osamu
Publication year - 1997
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.61.2.133
Subject(s) - biology , legionella pneumophila , intracellular , virology , multiplication (music) , microbiology and biotechnology , virus , monocyte , immunology , bacteria , genetics , physics , acoustics
Intracellular growth patterns of Legionella pneumophila were examined In monocytes obtained from carriers of human T‐lymphotropic virus type I (HTLV‐1) and controls who were HTLV‐1 seronegative. All subjects were seronegative for antibodies against L. pneumophila . Bacterial growth was determined 0, 1, 2, and/or 3 days after infecting peripheral blood mononuclear cells (PBMCs) with the bacteria. The intracellular growth of L. pneumophila was markedly inhibited in HTLV‐1 carriers compared with normal controls. When the lymphocytes were depleted from the HTLV‐1 carrier PBMC cultures before infection, this inhibition was abolished. Inhibition reappeared, however, when the 72‐h culture supernatants of PBMCs from HTLV‐1 carriers were added to the lymphocyte‐depleted cultures. Culture supernatants of infected and uninfected PBMCs from HTLV‐1 carriers exhibited markedly increased levels of interferon‐γ (IFN‐γ) and tumor necrosis factor α (TNF‐α) compared with the HTLV‐1 seronegative controls. In the HTLV‐1 carriers, IFN‐γ was produced by the CD4 + lymphocytes, whereas TNF‐α was secreted by the monocytes. Addition of anti‐IFN‐γ or anti‐TNF‐α antibodies to the HTLV‐1 carrier PBMC cultures diminished the inhibition of intracellular growth of L. pneumophila . Results suggest that the monocytes are activated in HTLV‐1 carriers. These findings may explain why an opportunistic infection by certain intracellular pathogens is rarely seen among HTLV‐1 carriers. J. Leukoc. Biol . 61: 133–140; 1997.