title: Marked inhibition of the intracellular multiplication of Legionella pneumophila in monocytes isolated from carriers of human T lymphotrophic virus type I.
abstract: 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-gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) compared with the HTLV-1 seronegative controls. In the HTLV-1 carriers, IFN-gamma was produced by the CD4+ lymphocytes, whereas TNF-alpha was secreted by the monocytes. Addition of anti-IFN-gamma or anti-TNF-alpha 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.
authors.affiliation: Department of Internal Medicine, Saga Medical School, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Funai
authors.forename: Y
authors.initials: Y
authors.lastname: Shimamoto
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.forename: S I
authors.initials: SI
authors.lastname: Yoshida
authors.forename: O
authors.initials: O
authors.lastname: Kohashi
mesh_terms: D000328:Adult; D000368:Aged; D002353:Carrier State / Q000276:immunology / Q000382:microbiology* / Q000821:virology*; D002469:Cell Separation; D016207:Cytokines / Q000096:biosynthesis; D015480:Deltaretrovirus Antibodies / Q000097:blood; D005260:Female; D015490:HTLV-I Infections / Q000276:immunology / Q000382:microbiology* / Q000821:virology; D006801:Humans; D007371:Interferon-gamma / Q000502:physiology; D007424:Intracellular Fluid / Q000276:immunology / Q000382:microbiology / Q000821:virology; D016952:Legionella pneumophila / Q000254:growth & development* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000382:microbiology* / Q000821:virology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D016207:Cytokines; D015480:Deltaretrovirus Antibodies; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma