Morphology of pulmonary intravascular macrophages (PIMs) in ruminants: Ultrastructural and cytochemical behavior of dense surface coat

Abstract

Recent studies have indicated that pulmonary intravascular macrophages (PIMs) are a resident cell population which in structure and function resemble mature macrophages of the mononuclear phagocyte system (MPS) in various domestic species, particularly the ruminants. The ultrastructural features of PIMs of the goat and calf lungs were studied by using vascular perfusion and direct airway instillation of fixatives. Staining with tannic acid as a component of paraformaldehyde-glutaraldehydebased fixative revealed the presence of an electron-dense coat on the surface of the cell membrane of the PIMs. The surface coat disappeared after heparin infusion and after enzymatic digestion with lipolytic lipase, suggesting that the surface coat was predominantly lipoprotein in nature. The lipoprotein coat was organized in the form of a linear chain of spherical globules with a consistent periodicity created by the intervening translucent space between individual globules. The surface coat was separated from the outerleaflet of the cell membrane by an empty space measuring 35-39 nm in width. P I M s possessed a significant number of coated pits and coated vesicles, the cell organelles of receptor-mediated endocytosis of lipoproteins. In concurrence with the coated pits and vesicles, microtubules, multivesicular bodies, and lipoprotein-positive vesicles were also observed. It is conceivable that PIMs are involved in lipid metabolism and are the major source of vasoactive substances, which significantly influence both the dynamics of pulmonary circulation and the surfactant turnover of the ruminant lung.

Immunophenotypic characterization and depletion of pulmonary intravascular macrophages of horses

“…PIMs differentiate from monocytes in post-natal life and form firm adhesions with the capillary endothelium [15,[36][37][38]. These cells phagocytize blood-born tracer particles, bacteria and endotoxins [3,18,27,29,36]. PIMcontaining species show pulmonary hypertension following the administration of tracer particles and endotoxins, and the removal of PIMs suppresses these responses 40 O.P.…”

Estrogen-induced microvilli and microvillar channels and entrapment of surfactant-lipids by alveolar type I cells of bovine lung

“…1). The PIMs presented their typical subcellular features particularly the globularsurface coat and a usual distribution of lysosomal particles (Atwal et al, 1989(Atwal et al, , 1992.…”

“…We have earlier suggested that TCER was most conspicuous in the adult female goat as compared to young goats of both sexes (Atwal, 1988;Atwal et al, 1990). Secondly, our purpose was to assess the effect of estrogen on the pulmonary intravascular macrophages, which are under on-going investigation in our laboratory over the last several years (Atwal et al, 1989(Atwal et al, , 1992a(Atwal et al, ,b, 1994Atwal and Minhas, 1992;Singh and Atwal, 1997). The estrogen in the past is known to cause marked changes in the number and function of cells of reticuloendothelial system which in recent years has been re-designated as Mononuclear Phagocyte System (MPS; Heller, 1957;Atwal, 1969;Loose et al, 1976;Boorman et al, 1980).…”

In vivo interaction of pulmonary intravascular macrophages with activated platelets in microvessels of equine lung after multiple exposures to halothane, isoflurane, and thiamylal: A comparative ultrastructural and cytochemical study

“…In previous studies, we tested the hypothesis that coat was predominantly composed of lipoproteins (LDL) by using an intravenous perfusion of heparin in goats, calves, and sheep (Atwal et al, 1989;Singh et al, 1995). We also applied the conventional technique of histochemistry for LDL by in vitro digestion of lung slices in lipolytic lipase (LPL) solution.…”

“…Both experimental procedures potentiated the disappearance of the coat from the surface and its subsequent translocation into the vacuolar system of the PIMs. These physiological and cytochemical changes were attributed to the lytic effects of LPL, mobilized from the extracellular matrix of the pulmonary endothelium and/or secreted by the PIMs (Atwal et al, 1989;Singh et al, 1995). The intracellular translocation of the coat globules was explained by assuming that LPL/LDL complexes were internalized by the PIMs upon binding to plasma membrane-associated heparin sulfate, an interaction that is heparin-sensitive under physiological conditions (Schön-herr et al, 2000).…”