Macrophage nitric oxide synthase (NOS) activation by Nocardia opaca fractions and 15‐ and 56‐kD isolated antigens
The Gram‐positive bacterium, Nocardia opaca, is a source of substances with adjuvant effect, ability to stimulate macrophages and natural killer cells for enhanced cytotoxity and cytokine production and B lymphocytes for polyclonal immunoglobulin secretion. We determined the immunogenicity of isolat...
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Published in | Clinical and experimental immunology Vol. 104; no. 2; pp. 215 - 220 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford BSL
Blackwell Science Ltd
01.05.1996
Blackwell Blackwell Science Inc |
Subjects | |
Online Access | Get full text |
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Summary: | The Gram‐positive bacterium, Nocardia opaca, is a source of substances with adjuvant effect, ability to stimulate macrophages and natural killer cells for enhanced cytotoxity and cytokine production and B lymphocytes for polyclonal immunoglobulin secretion. We determined the immunogenicity of isolated N. opaca fractions and prepared MoAbs against immunogenic water‐soluble mitogen (NWSM). Two main proteins of molecular mass 15 and 56 kD were detected in Western blot analysis and isolated by affinity chromatography using anti‐NWSM MoAb B7/7. Both these isolated nocardial antigens were found to stimulate mouse peritoneal macrophage NOS. The effect of 5 μg NWSM was comparable to that of 5 μg lipopolysaccharide (LPS) or 20 U of interferon‐gamma (IFN‐γ) added to cell cultures. The MoAb B7/7 decreased NO−2 production induced by NWSM or by isolated nocardial antigens, but did not significantly influence the production elicited by LPS or IFN‐γ. On the other hand, NOS activation by NWSM was not affected by anti‐IFN‐γ MoAb. The possible independent pathway for IFN‐γ and NWSM macrophage activation is discussed. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0009-9104 1365-2249 |
DOI: | 10.1046/j.1365-2249.1996.23730.x |