Alveolar macrophage phagocytosis

Schagat, T.L., Wofford, J.A., and Wright, J.R., Surfactant protein A enhances alveolar macrophage phagocytosis of apoptotic neutrophils, J. Immunol. 166, 4, 2727, 2001. 

Renwick, L. C., Donaldson, K., and Clouter, A. Impairment of alveolar macrophage phagocytosis by ultrafine particles. Toxicol. Appl. Pharmacol. 172 119-127, 2001. 

Jakob GJ, Hemenway DR. Concomitant exposure to carbon black particulates enhance ozone-induced lung inflammation and suppression of alveolar macrophage phagocytosis. J Toxicol Environ Health 1994 41 221-231. 

Jakab GJ. Relationship between carbon black particulate-bound formaldehyde, pulmonary antibacterial defenses, and alveolar macrophage phagocytosis. Inhal Toxicol 1992 4 325-342. 

Jakab GJ, Hemenway DR. Inhalation co-exposure to carbon black and acrolein suppresses alveolar macrophage phagocytosis and TNF-a release and modulates peritoneal macrophage phagocytosis. Inhal Toxicol 1993 5 275-289. 

Damon, M., Cluzel, M., Chanez, P. and Goddard, P. (1989). Phagocytosis induction of chemiluminescence and chemoattractant-increased superoxide anion release from activated human alveolar macrophages in asthma. J. Biolumin. Chemolumin. 4, 279-286. 

Taya A, Carmack DB, Muggenburg BA, et al. 1992. An interspecies comparison of the phagocytosis and dissolution of 241Am02 particles by rat, dog and monkey alveolar macrophages in vitro. Int J Radiat Biol 62(l) 89-95. 

FI G U RE 10.2 Schematic representation of alveolar cells and possible mechanism of transport of molecules from the alveolar space into the circulation. Particles will release molecules of interest (gray circles) into the mucus in which the particle is embedded. The molecule can either be lost in the mucus, taken up by alveolar macrophages by phagocytosis or diffusion, taken up by alveolar epithelial cells by passive or active transport, or bypass the alveolar cells via paracellular transport depending upon the properties of the drug. Once a molecule has reached the extracellular space, the same mechanisms are possible for transport from the extracellular space into the blood. Molecules in the extracellular space may also reach to circulation via the lymph. 

Low ES, Low RB, Green GM. 1977. Correlated effects of cigarette smoke components on alveolar macrophage adenosine triphosphatase activity and phagocytosis. Am Rev Respir Dis 115 963-970. 

After binding and phagocytosis, alveolar macrophages and monocytes release pro-inflammatory cytokines, e.g. lL-1, interferon-y and tumor necrosis factor-a (fig. 1). These cytokines activate resident cells (epithelial cells, fibroblasts) to produce chemokines such as lL-8, granulocyte-monocyte-colony-stimulating factor, RANTES (regulated on activation normal T cell expressed and secreted) that will result in a second wave of cell recruitment (mononuclear and polymorphonuclear cells). 

Alveolar macrophages migrate along the alveolar wall to engulf spores by phagocytosis in phagolysosomes. 

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