Macrophages, reactive nitrogen species, and lung injury

Rutgers University, Piscataway, New Jersey, USA.
Annals of the New York Academy of Sciences (Impact Factor: 4.38). 08/2010; 1203(1):60-5. DOI: 10.1111/j.1749-6632.2010.05607.x
Source: PubMed


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.

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    PLoS ONE 10/2013; 8(10):e77002. DOI:10.1371/journal.pone.0077002 · 3.23 Impact Factor
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    • "Macrophages play a key role in the immune response being the first cells to be exposed to microorganisms. These cells are considered as sentinel cells against infectious pathogens and involved in phagocytosis, antigen presentation, production of antimicrobial effector molecules and release of cytokines and chemokines that in turn contribute to immune cell recruitment and activation [18-20]. The recognition of microorganisms by macrophages occurs through a major receptor family expressed in distinct cell subsets and tissues called the Toll-Like Receptors (TLR) [21-23]. "
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