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Role of IFN‐γ on dissociation between nitric oxide and TNF/IL‐6 production by murine peritoneal cells after restimulation with bacterial lipopolysaccharide
Author(s) -
Tominaga Kaoru,
Saito Shinji,
Matsuura Motohiro,
Funatogawa Keiji,
Matsumura Haruo,
Nakano Masayasu
Publication year - 1999
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.66.6.974
Subject(s) - lipopolysaccharide , nitric oxide , tumor necrosis factor alpha , biology , interferon gamma , antibody , interleukin , interferon , cytokine , immunology , microbiology and biotechnology , endocrinology
Murine peritoneal exudate cells (PEC) pre‐exposed to bacterial lipopolysaccharide (LPS) show augmented nitric oxide (NO) production by LPS restimulation, in contrast to LPS tolerance with reduced production of tumor necrosis factor α (TNF‐α) and interleukin‐6 (IL‐6). Significant amounts of interferon‐γ (IFN‐γ) were detected in the PEC cultures on LPS stimulation, and anti‐IFN‐γ antibody suppressed the LPS‐induced NO, but not TNF‐α and IL‐6, production. Addition of anti‐IFN‐γ antibody to the cultures in the LPS pre‐exposure step strongly suppressed the augmented NO production on LPS restimulation. Anti‐IL‐12 antibody, which suppressed the LPS‐induced IFN‐γ production, also suppressed the augmented NO production, as did anti‐IFN‐γ antibody. Taken together, we propose the following mechanisms: (1) T and NK cells in PEC produce IFN‐γ by the action of IL‐12, which is derived from LPS‐stimulated macrophages, and (2) the de novo ‐produced IFN‐γ activates macrophages to augment NO production on LPS restimulation. J. Leukoc. Biol. 66: 974–980; 1999.