Abstract
Phagocytic mononuclear cells respond to tissue injury and infection with the upregulation of cell surface markers, the production of inflammatory and anti-microbial mediators, and through their early mobilization. These cells initiate and resolve inflammation as well as participate in tissue remodeling and repair. Within various tissues, including the heart and lung, cross-talk between epithelial and endothelial cells and macrophage/monocytes is critical for both maintaining the resting, steady-state, and in coordinating response to insult. Macrophages and monocytes display high functional plasticity, altering their phenotype and activity in response to changing conditions within their microenvironment.
A feature of advancing age is elevated basal levels of proinflammatory cytokines and other indicators of chronic inflammation, a phenomenon termed “inflamm-aging.” The accumulation of senescent cells within the tissues is the likely source of these inflammatory markers, as senescence, a state of irreversible inhibition of cell proliferation, results in alteration of the cellular secretory profile as well. This altered microenvironmental state affects the functionality of tissue resident macrophages and monocytes, skewing their responses to injury or infection. Cell-inherent age-associated alterations in functional potential are superimposed on these changes within the tissue milieu. Here we discuss the phagocytic mononuclear cell populations of two tissues, the heart and lungs, their origin, phenotypes, and function during the steady state and following insult and how advancing age impacts their function.
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Thoman, M., Bray, W., Linton, PJ. (2019). Monocytes and Macrophages in the Aged Lung and Heart. In: Fulop, T., Franceschi, C., Hirokawa, K., Pawelec, G. (eds) Handbook of Immunosenescence. Springer, Cham. https://doi.org/10.1007/978-3-319-99375-1_94
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