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Interleukin-1-mediated acute lung injury and tolerance to oxidative injury.
Interleukin-1 (IL-1) is a highly potent molecule that has a myriad of effects in biologic systems. This brief review describes some of our findings on the effects of IL-1 in biologic systems. On the one hand, IL-1 treatment caused a neutrophil-dependent acute edematous lung injury that resembled cha...
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Formato: | Texto |
Lenguaje: | English |
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1994
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566998/ https://www.ncbi.nlm.nih.gov/pubmed/7705311 |
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author | Repine, J E |
author_facet | Repine, J E |
author_sort | Repine, J E |
collection | PubMed |
description | Interleukin-1 (IL-1) is a highly potent molecule that has a myriad of effects in biologic systems. This brief review describes some of our findings on the effects of IL-1 in biologic systems. On the one hand, IL-1 treatment caused a neutrophil-dependent acute edematous lung injury that resembled changes in the lungs of patients with the acute respiratory distress syndrome (ARDS). On the other hand, IL-1 pretreatment conferred a tolerance to lung oxidative lung injury and ischemia-reperfusion insults--again conditions manifest in sick patients. The potential mechanisms responsible for these seemingly paradoxical influences of IL-1 are described and related to possible strategies for the treatment of patients with ARDS, ischemia-reperfusion disorders, and other oxidant-mediated conditions. |
format | Text |
id | pubmed-1566998 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1994 |
record_format | MEDLINE/PubMed |
spelling | pubmed-15669982006-09-19 Interleukin-1-mediated acute lung injury and tolerance to oxidative injury. Repine, J E Environ Health Perspect Research Article Interleukin-1 (IL-1) is a highly potent molecule that has a myriad of effects in biologic systems. This brief review describes some of our findings on the effects of IL-1 in biologic systems. On the one hand, IL-1 treatment caused a neutrophil-dependent acute edematous lung injury that resembled changes in the lungs of patients with the acute respiratory distress syndrome (ARDS). On the other hand, IL-1 pretreatment conferred a tolerance to lung oxidative lung injury and ischemia-reperfusion insults--again conditions manifest in sick patients. The potential mechanisms responsible for these seemingly paradoxical influences of IL-1 are described and related to possible strategies for the treatment of patients with ARDS, ischemia-reperfusion disorders, and other oxidant-mediated conditions. 1994-12 /pmc/articles/PMC1566998/ /pubmed/7705311 Text en |
spellingShingle | Research Article Repine, J E Interleukin-1-mediated acute lung injury and tolerance to oxidative injury. |
title | Interleukin-1-mediated acute lung injury and tolerance to oxidative injury. |
title_full | Interleukin-1-mediated acute lung injury and tolerance to oxidative injury. |
title_fullStr | Interleukin-1-mediated acute lung injury and tolerance to oxidative injury. |
title_full_unstemmed | Interleukin-1-mediated acute lung injury and tolerance to oxidative injury. |
title_short | Interleukin-1-mediated acute lung injury and tolerance to oxidative injury. |
title_sort | interleukin-1-mediated acute lung injury and tolerance to oxidative injury. |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566998/ https://www.ncbi.nlm.nih.gov/pubmed/7705311 |
work_keys_str_mv | AT repineje interleukin1mediatedacutelunginjuryandtolerancetooxidativeinjury |