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Increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysaccharide

After in vitro exposure to lipopolysaccharide (LPS) or muramyl dipeptide (MDP), cultured resident mouse peritoneal macrophages were primed to display enhanced generation of superoxide anion (O2-) in response to stimulation by phorbol myristate acetate (PMA) or opsonized zymosan. Priming with LPS (1...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1980
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2185752/
https://www.ncbi.nlm.nih.gov/pubmed/7350246
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description After in vitro exposure to lipopolysaccharide (LPS) or muramyl dipeptide (MDP), cultured resident mouse peritoneal macrophages were primed to display enhanced generation of superoxide anion (O2-) in response to stimulation by phorbol myristate acetate (PMA) or opsonized zymosan. Priming with LPS (1 microgram/ml) produced a sevenfold enhancement of PMA-stimulated O2- generation; priming was detected within 30 min and persisted for at least 4 d. Exposure to MDP (1 muM) primed the macrophages to double their O2- release; the response was first observed after 4 h and persisted for at least 3 d. The priming response was not observed with stereoisomers of MDP, which are inactive as adjuvants. LPS and MDP appeared to work directly on the macrophages rather than indirectly by interacting with adherent lymphocytes: (a) Addition of nonadherent cell populations that contained lymphocytes had no effect on the response. (b) The response was normal with cells from nude mice, which lack mature T lymphocytes. (c) Macrophages from C3H/HeJ mice, whose B lymphocytes fail to respond to LPS, were weak in their response to priming LPS; the addition of normal (C3Heb/FeJ) nonadherent cells had no effect on this weak response. (d) The macrophage-like cell line J774.1 also showed enhanced O2--generating capacity after a 4-h exposure to LPS or MDP. The O2--generating capacity of macrophages primed with LPS in vitro was equivalent to that previously observed with cells elicited in vivo by injection of LPS or activated by infection with Bacille Calmette-Guerin. The data suggest that previous exposure to bacterial products could prime macrophages to respond with increased production of toxic oxygen metabolites on contact with invading microorganisms or tumor cells.
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spelling pubmed-21857522008-04-17 Increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysaccharide J Exp Med Articles After in vitro exposure to lipopolysaccharide (LPS) or muramyl dipeptide (MDP), cultured resident mouse peritoneal macrophages were primed to display enhanced generation of superoxide anion (O2-) in response to stimulation by phorbol myristate acetate (PMA) or opsonized zymosan. Priming with LPS (1 microgram/ml) produced a sevenfold enhancement of PMA-stimulated O2- generation; priming was detected within 30 min and persisted for at least 4 d. Exposure to MDP (1 muM) primed the macrophages to double their O2- release; the response was first observed after 4 h and persisted for at least 3 d. The priming response was not observed with stereoisomers of MDP, which are inactive as adjuvants. LPS and MDP appeared to work directly on the macrophages rather than indirectly by interacting with adherent lymphocytes: (a) Addition of nonadherent cell populations that contained lymphocytes had no effect on the response. (b) The response was normal with cells from nude mice, which lack mature T lymphocytes. (c) Macrophages from C3H/HeJ mice, whose B lymphocytes fail to respond to LPS, were weak in their response to priming LPS; the addition of normal (C3Heb/FeJ) nonadherent cells had no effect on this weak response. (d) The macrophage-like cell line J774.1 also showed enhanced O2--generating capacity after a 4-h exposure to LPS or MDP. The O2--generating capacity of macrophages primed with LPS in vitro was equivalent to that previously observed with cells elicited in vivo by injection of LPS or activated by infection with Bacille Calmette-Guerin. The data suggest that previous exposure to bacterial products could prime macrophages to respond with increased production of toxic oxygen metabolites on contact with invading microorganisms or tumor cells. The Rockefeller University Press 1980-01-01 /pmc/articles/PMC2185752/ /pubmed/7350246 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysaccharide
title Increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysaccharide
title_full Increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysaccharide
title_fullStr Increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysaccharide
title_full_unstemmed Increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysaccharide
title_short Increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysaccharide
title_sort increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysaccharide
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2185752/
https://www.ncbi.nlm.nih.gov/pubmed/7350246