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Interleukin-7 Induces Anti-Mycobacterium avium Activity in Human Monocyte Derived Macrophages
Author(s) -
T. Tantawichien,
Lawrence S. Young,
L. E. Bermudez
Publication year - 1996
Publication title -
the journal of infectious diseases
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1093/infdis/174.3.574
Subject(s) - microbiology and biotechnology , secretion , macrophage , tumor necrosis factor alpha , antimycobacterial , cytokine , intracellular , immune system , biology , macrophage activating factor , monocyte , mycobacterium , interleukin , transforming growth factor , immunology , bacteria , medicine , lymphokine , in vitro , mycobacterium tuberculosis , biochemistry , endocrinology , pathology , tuberculosis , genetics
To examine the modulatory role of interleukin (IL)-7 on intracellular growth of Mycobacterium avium complex (MAC), human macrophages were treated either before or after MAC infection with different concentrations of IL-7. At 100 pg/mL, 1 ng/mL, and 10 ng/mL, treatment with IL-7 before infection stimulated secretion of tumor necrosis factor-alpha (TNF-alpha) from MAC-infected macrophages (increase up to 40%) and resulted in dose-dependent reduction in the number of intracellular bacteria. Pretreatment with IL-7 did not inhibit the secretion of transforming growth factor-beta1 (TGF-beta1). IL-7 added to the macrophage monolayer 4 h after infection resulted in both the secretion of TNF-alpha from MAC-infected macrophages (up to 90% increase, P < .05) and antimycobacterial activity (up to 50% reduction in bacteria, P <.05); however, TGF-beta1 production was not inhibited. IL-7-dependent anti-MAC activity of macrophages was inhibited by anti-human TNF-alpha antibody. These results suggest that IL-7 may contribute to the regulation of the immune response against MAC.

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