Macrophage functions and persistence in chronic inflammation
THE CONTEXT
Activated macrophages help eliminate injurious agents and initiate repair, while also causing much of the tissue injury in chronic inflammation.
Histologic contrast in the lung
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Chronic inflammation shows collections of chronic inflammatory cells, destruction of parenchyma, and replacement by connective tissue through fibrosis.
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In the illustrated chronic lung lesion, normal alveoli are replaced by spaces lined by cuboidal epithelium.
Macrophages ingest and eliminate microbes and debris from dead tissues.
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They secrete inflammatory mediators, including TNF, IL-1, chemokines, and eicosanoids, contributing to initiation and propagation of inflammation.
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They initiate tissue repair, scar formation, and fibrosis.
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They display antigens to T lymphocytes and respond to T-cell signals, creating a feedback loop essential for cell-mediated defense against many microbes.
Persistence and activation patterns
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After the irritant is eliminated, macrophages usually disappear by dying or traveling through lymphatics to lymph nodes.
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Persistent accumulation can result from continued recruitment from the circulation and local proliferation at the inflammatory site.
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A precise sequence from classical activation to alternative activation is not well documented in most inflammatory reactions.
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M1 and M2 are useful conceptual phenotypes, but additional macrophage subpopulations represent intermediates between them.