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Interaction with vesicular stomatitis virus‐infected BALB/c3T3 cells inhibits the synthesis of nitric oxide in activated murine bone marrow culture‐derived macrophages
Author(s) -
Crowder Chun W.,
Murphy William J.,
Russell Stephen W.,
LeBlanc Paul A.
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.65.5.605
Subject(s) - vesicular stomatitis virus , biology , nitric oxide synthase , nitric oxide , microbiology and biotechnology , macrophage , lipopolysaccharide , 3t3 cells , transfection , cell culture , interferon gamma , bone marrow , virus , virology , immunology , cytokine , biochemistry , in vitro , endocrinology , genetics
Bone marrow‐culture‐derived macrophages activated with interferon‐γ and lipopolysaccharide produced less nitric oxide (NO) when cultured with vesicular stomatitis virus (VSV)‐infected BALB/c3T3 (3T3‐VSV) than macrophages activated in an identical manner and cultured alone, with uninfected BALB/c3T3 (3T3), or with P815. However, all four groups of macrophages produced nearly the same amount of interleukin‐6 (IL‐6). Addition of VSV to activated macrophages did not change the amount of NO produced. The amount of NO generated by two non‐macrophage sources of NO was not affected by the presence of either P815 or 3T3‐VSV. Reverse transcriptase‐polymerase chain reaction showed a decrease in the amount of inducible nitric oxide synthase (iNOS) but not IL‐6 mRNA from macrophages cocultured with 3T3‐VSV compared with macrophages cocultured with P815. The reduction in iNOS mRNA was confirmed by ribonuclease protection assay. When RAW 264.7 transfected with an iNOS regulatory construct were activated and incubated with 3T3‐VSV there was a decrease in the expression of the reporter luciferase gene and NO production but not IL‐6 production compared with cells incubated with either medium alone or with P815. J. Leukoc. Biol. 65: 605–613; 1999.

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