Literature DB >> 3284325

Pulmonary intravascular macrophages in domestic animal species: review of structural and functional properties.

G C Winkler1.   

Abstract

In dogs, laboratory animals, and man, the clearance of bacteria and particulates from blood occurs predominantly in hepatic Kupffer cells and splenic macrophages. In contrast, removal of blood-borne particulates in calves, sheep, goats, cats, and pigs occurs predominantly in pulmonary intravascular macrophages (PIMs). Review of recent studies indicates that PIMs are a resident cell population, junctionally adherent to the capillary endothelium of lungs and morphologically similar to hepatic Kupffer cells. PIMs are a pulmonary constituent of the mononuclear phagocyte system with respect to secretory, endocytic, and functional properties. Differentiated PIMs are rare in newborn pigs, and the majority of cells closely apposed to capillary endothelium consists of monocytes, which are occasionally in mitosis. In 7-day-old and older pigs, most cells apposed to capillary endothelium have characteristics of differentiated PIMs. This suggests a monocytic origin of PIMs in pigs. Perinatal colonization of lung capillaries by monocytes and their subsequent differentiation into PIMs represent a component of postnatal lung development. Estimates of relative PIM numbers in ovine and porcine lung parenchyma suggest cell densities similar to that of rat hepatic Kupffer cells. Apart from phagocytic properties, PIMs participate in the removal and disintegration of aged and impaired blood cells. After phagocytic stimulation, isolated PIMs secrete oxygen radicals, which are essential for microbicidal function. Similarly, by secreting bioactive lipids, stimulated PIMs may contribute to regulation of pulmonary hemodynamics. After receiving minute amounts of bacterial endotoxin, pulmonary injury is pronounced in sheep, calves, pigs, and cats, but not in laboratory animals and dogs. This presumably is related to the secretion of bioactive lipids by PIMs.

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Year:  1988        PMID: 3284325     DOI: 10.1002/aja.1001810302

Source DB:  PubMed          Journal:  Am J Anat        ISSN: 0002-9106


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