Macrophages and inflammatory mediators in chemical toxicity: a battle of forces.

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2009 Aug;22(8):1376-85.

Macrophages and inflammatory mediators in chemical toxicity: a battle of forces.

Laskin DL.

Department of Pharmacology and Toxicology, Rutgers University, Ernest

School of Pharmacy, Piscataway, New Jersey 08854.

Abstract

Macrophages function as control switches of the immune system, providing a

balance between pro- and anti-inflammatory responses. To accomplish this, they

develop into different subsets: classically (M1) or alternatively (M2) activated

macrophages. Whereas M1 macrophages display a cytotoxic, proinflammatory

phenotype, much like the soldiers of The Dark Side of The Force in the Star Wars

movies, M2 macrophages, like Jedi fighters, suppress immune and inflammatory

responses and participate in wound repair and angiogenesis. Critical to the

actions of these divergent or polarized macrophage subpopulations is the

regulated release of inflammatory mediators. When properly controlled, M1

macrophages effectively destroy invading pathogens, tumor cells, and foreign

materials. However, when M1 activation becomes excessive or uncontrolled, these

cells can succumb to The Dark Side, releasing copious amounts of cytotoxic

mediators that contribute to disease pathogenesis. The activity of M1

macrophages is countered by The Force of alternatively activated M2 macrophages,

which release anti-inflammatory cytokines, growth factors, and mediators

involved in extracellular matrix turnover and tissue repair. It is the balance

in the production of mediators by these two macrophage subpopulations that

ultimately determines the outcome of the tissue response to chemical toxicants.

http://www.ncbi.nlm.nih.gov/pubmed/19645497

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2787782/?tool=pubmed