Macrophages, reactive nitrogen species, and lung injury

Debra L. Laskin, Vasanthi R. Sunil, Ladan Fakhrzadeh, Angela Groves, Andrew J. Gow, Jeffrey D. Laskin

Результат исследований: Материалы для книги/типы отчетовМатериалы для конференции

24 Цитирования (Scopus)

Аннотация

Evidence has accumulated over the past several years demonstrating that lung injury following inhalation of irritants like ozone is due, not only to direct effects of the chemical, but also indirectly to the actions of inflammatory mediators released by infiltrating macrophages. Among the mediators involved in the cytotoxic process, reactive nitrogen species (RNS) are of particular interest because of their well-documented cytotoxic potential. Findings that macrophage suppression blocks RNS production and ozone-induced toxicity provide strong support for a role of these cells and inflammatory mediators in lung injury. Recent investigations have focused on understanding pathways by which macrophages become activated to release RNS. One protein that has attracted considerable attention is caveolin-1, a membrane scaffolding molecule that functions to negatively regulate cell signaling. The fact that expression of caveolin-1 is down-regulated in macrophages after ozone inhalation suggests a mechanism controlling the release of cytotoxic mediators by these inflammatory cells.

Язык оригиналаАнглийский
Название основной публикацииOxidative/Nitrosative Stress and Disease
Страницы60-65
Число страниц6
Том1203
DOI
СостояниеОпубликовано - авг 2010
Опубликовано для внешнего пользованияДа

Серия публикаций

НазваниеAnnals of the New York Academy of Sciences
Том1203
ISSN (печатное издание)00778923
ISSN (электронное издание)17496632

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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