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Oxygen radicals, cytokines, adhesion molecules, and lung injury.

Inflammatory injury in the lung or dermis occurring after systemic activation of complement or after local deposition of immune complexes is related to local activation of tissue macrophages and/or recruitment of blood neutrophils. While requirements for cytokines (IL-1, TNF alpha, MCP-1) vary with...

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Detalles Bibliográficos
Autor principal: Ward, P A
Formato: Texto
Lenguaje:English
Publicado: 1994
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566973/
https://www.ncbi.nlm.nih.gov/pubmed/7705287
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author Ward, P A
author_facet Ward, P A
author_sort Ward, P A
collection PubMed
description Inflammatory injury in the lung or dermis occurring after systemic activation of complement or after local deposition of immune complexes is related to local activation of tissue macrophages and/or recruitment of blood neutrophils. While requirements for cytokines (IL-1, TNF alpha, MCP-1) vary with the model of injury, requirements for adhesion molecules (beta 2 integrins, selectins, ICAM-1) differ. In most cases the immediate events related to tissue injury can be linked to toxic products from oxygen and L-arginine. Whether there is a single toxic product or a variety of toxic products remains to be determined. These data emphasize similarities and differences in the mechanisms of inflammatory injury, as a function of the inciting inflammatory agent and the organ system involved.
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spelling pubmed-15669732006-09-19 Oxygen radicals, cytokines, adhesion molecules, and lung injury. Ward, P A Environ Health Perspect Research Article Inflammatory injury in the lung or dermis occurring after systemic activation of complement or after local deposition of immune complexes is related to local activation of tissue macrophages and/or recruitment of blood neutrophils. While requirements for cytokines (IL-1, TNF alpha, MCP-1) vary with the model of injury, requirements for adhesion molecules (beta 2 integrins, selectins, ICAM-1) differ. In most cases the immediate events related to tissue injury can be linked to toxic products from oxygen and L-arginine. Whether there is a single toxic product or a variety of toxic products remains to be determined. These data emphasize similarities and differences in the mechanisms of inflammatory injury, as a function of the inciting inflammatory agent and the organ system involved. 1994-12 /pmc/articles/PMC1566973/ /pubmed/7705287 Text en
spellingShingle Research Article
Ward, P A
Oxygen radicals, cytokines, adhesion molecules, and lung injury.
title Oxygen radicals, cytokines, adhesion molecules, and lung injury.
title_full Oxygen radicals, cytokines, adhesion molecules, and lung injury.
title_fullStr Oxygen radicals, cytokines, adhesion molecules, and lung injury.
title_full_unstemmed Oxygen radicals, cytokines, adhesion molecules, and lung injury.
title_short Oxygen radicals, cytokines, adhesion molecules, and lung injury.
title_sort oxygen radicals, cytokines, adhesion molecules, and lung injury.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566973/
https://www.ncbi.nlm.nih.gov/pubmed/7705287
work_keys_str_mv AT wardpa oxygenradicalscytokinesadhesionmoleculesandlunginjury