Open AccessRecombinant granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) or tumour necrosis factor‐alpha (TNF‐α) activate human alveolar macrophages to inhibit growth of Mycobacterium avium complex
Author(s) -
SUZUKI K.,
LEE W. J.,
HASHIMOTO T.,
TANAKA E.,
MURAYAMA T.,
AMITANI R.,
YAMAMOTO K.,
KUZE F.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb06625.x
Subject(s) - cytokine , tumor necrosis factor alpha , macrophage , phagocytosis , recombinant dna , interferon gamma , granulocyte macrophage colony stimulating factor , macrophage activating factor , biology , immunology , chemistry , in vitro , biochemistry , gene
Summary We investigated the effects of certain macrophage‐active cytokines on the phagocytosis and growth inibition of Mycobacterium avium complex (MAC) by human alveolar macrophages (AM). We also evaluated the effects of pretreatment with each cytokine on the superoxide anion release (O 2 ‐ ) from AM. The cytokines that we used were recombinant GM‐CSF, natural type TNF‐α, recombinant interferon‐gamma (IFN‐γ). and recombinant IL‐2, We found that phagocytosis by the various cytokine‐stimulated AM was similar lo that of unstimulated AM. On the other hand, significant growth inhibition of MAC was observed in the macrophages treated with GM‐CSF or TNF‐α, while no growth inhibition of MAC was observed in the macrophages treated with IF'N‐γ or IL‐2. Pretreatment with alt cytokines tested enhanced the O 2 ‐ release from AM. but there was no correlation between the enhancement of O 2 ‐ release and the growth inhibition of MAC, Thus, we concluded that GM‐CSF or TNF‐α could activate AM to inhibit growth of MAC, probably not through the enhanced production of reactive oxygen intermediates.