Human alveolar macrophages spontaneous reduction of BSPT salt

Summary Alveolar macrophages of non smoking and smoking human adults reduce BSPT salt spontaneously. The staining obtained is located on three cell membrane systems: the endoplasmic reticulum, the Golgi apparatus and the nuclear envelope. Methylene blue MB inhibits BSPT reduction. The smokers alveolar macrophages have less positivity than those of the non smokers. The endogenous cell substrate revealed in this work is the initial common pathway of two different oxidative chains bounded to the microsome. One acts with cytochrome P 450 for chemical detoxification by hydroxylation, the other one acts with cytochrome B₅ for lipid oxidation or peroxidation and both may be connected with the cell bactericidal system.     

Human alveolar macrophages: HLA-DR-positive macrophages that are poor stimulators of a primary mixed leukocyte reaction

Previous studies demonstrated that alveolar macrophages (AM) from most normal human volunteers failed to stimulate the antigen-induced proliferation of peripheral blood T lymphocytes although greater than 90% of AM expressed HLA-DR antigens. The current studies establish that AM also fail to induce allogeneic peripheral blood mononuclear cells to proliferate in a mixed leukocyte reaction (MLR). Suppressive activity by AM was not an explanation for their failure to induce an MLR. Indirect immunofluorescence established the presence of both HLA-DR and DQ antigens on the majority of AM and the persistence of these antigens on cells in culture for up to 6 days, the period of time required to observe a maximal MLR. Metabolic labeling experiments also demonstrated that HLA-DR antigens were synthesized by AM. It was recently reported that AM secrete relatively small amounts of IL 1, an important ancillary signal provided by accessory cells to enhance the stimulation of lymphocyte proliferation. However, addition of optimal concentrations of IL 1 to cultures containing AM failed to enhance the MLR. Thus, there is at least one additional, but as yet undefined, requirement for an accessory cell to induce an optimal MLR besides the display of HLA-D region antigens and the secretion of IL 1. In contrast, AM were effective in specifically stimulating proliferation of alloreactive T cell lines, suggesting that at least some cell lines do not require this nonspecific undefined second signal. We speculate that although AM may not initiate primary immune responses in the lung, they may be important in maintaining immune-mediated inflammatory responses by specifically restimulating already activated T cells.     

Chronic cigarette smoking enhances spontaneous release of tumour necrosis factor-alpha from alveolar macrophages of rats

Some biological effects of chronic cigarette smoking (two cigarettes for 2 h, daily for 4 months) in rats were evaluated. During the smoking period, body weight of smoker rats was always significantly lower than that of control rats. Immediately after the last smoking session the carboxyhaemoglobin concentration in the blood was about 8.5% and the polymorphonuclear cells in the bronchoalveolar fluid increased significantly. At the same time, enzymatic analyses on the supernatants of bronchoalveolar fluid revealed a significant increase of beta-glucuronidase in the smoker group. Alveolar macrophages, collected 0, 8 and 24 h after the last smoking session, significantly increased the generation of superoxide anion and, after incubation for 24 h at 37( degrees ) C in a humidified atmosphere, released significantly high amounts of TNF-alpha. When challenged with lipopolysaccharide, alveolar macrophages of smoker rats released much more TNF-alpha but, in such a case, TNF-alpha release was about one half of that observed in the control group. Peritoneal macrophages of both control and smoker rats were unable either to generate high levels of superoxide anion or to release significant amounts of TNF-alpha. The results clearly demonstrated the activated state of alveolar macrophages and the resting state of peritoneal macrophages.     

Production of interferon by alveolar macrophages

Acton, Jean D. (Bowman Gray School of Medicine, Winston-Salem, N.C.), and Quentin N. Myrvik. Production of interferon by alveolar macrophages. J. Bacteriol. 91:2300-2304. 1966.-Rabbit alveolar macrophages inoculated with parainfluenza-3 virus in vitro produce a viral inhibitor which possesses the properties of interferon. The interferon is nondialyzable, is stable at pH 4, is not sedimented at 100,000 x g, exhibits species specificity, and can passively protect other alveolar macrophages from infection with virulent rabbitpox virus. The possible significance of alveolar macrophage-produced interferon is discussed.     

Superoxide generation by pig alveolar macrophages

Pig alveolar macrophages generate superoxide anions at a rate of 1.8 nanomoles/1 X 10(6) cells/min. The intracellular value of ATP in resting cells was 4.0 +/- 0.1 X 10(-16) mole/cell; in contrast the value in cells generating superoxide anions was 2.0 +/- 0.6. Superoxide generation was increasingly inhibited by exposing cells to adenosine from 0.1 to 1.0 mM. Unlike human macrophages, pig cell production of superoxide anions was not inhibited by exposure to the adenosine analog, 2-Cl-adenosine.     

Architectonics of the surface of alveolar macrophages

The architectonics of the alveolar macrophage surface has been investigated in the raster electron microscope. The material is obtained by means of washing from the lungs of intact noninbred white rats and also 24 h after a single intragastric administration of a cancerogenic agent--nitrosodimethylamine (NDMA)--in a toxic dose (30 mg/kg). The alveolar macrophages are studied both as a suspension and also after 30 min of cultivation. The preparations are dried in the air and by the critical point method. When the latter method is used, the architectonics of the alveolar macrophage surface is much richer. Nevertheless, the former method also gives enough information. NDMA administration produces a damaging effect on the surface architectonics and on the character of the macrophages spreading over the glass. The morphological characteristics of the changes in the surface architectonics of the alveolar macrophages can be used to estimate the cytotoxic effect of different harmful factors of the environment.     

Effect of methimazole-induced hypothyroidism on alveolar macrophages

Chemically induced hypothyroidism changes the functions of rat alveolar macrophages. Treatment of female rats with an anti-thyroid drug, methimazole (1% aqueous solution in drinking water for 6 weeks) significantly (p less than 0.05) reduced the ability of alveolar macrophages (MAM) to phagocytose and kill the yeast, Saccharomyces cerevisiae. Undigested yeasts were observed in phagolysosomes within MAM using transmission electron microscopy. The activities of the lysosomal enzymes, acid phosphatase and beta-glucuronidase, and the Fc receptor binding ability for immunoglobulin G, were lowered in MAM when compared with control macrophages (CAM). MAM also produced less tumor necrosis factor under the stimulation of lipopolysaccharide.     

Phagocytosis of liposomes by human alveolar macrophages

The ability of cells recovered from lung lavages to phagocytose liposomes has been investigated.Inulin (¹⁴C-labelled), entrapped in multilamellar immunoglobulin-G coated liposomes with ³H-labelled cholesterol as the lipid phase marker, was fed to the recovered cells. Fifteen patients with diffuse interstitial pulmonary disease (DIPD), prior to steroid treatment, and eight normal controls were lavaged for the study. Uptake was found for both groups and it was concluded that the liposomes enter the cells predominantly via endocytosis. Follow-up lavage, three months after the initial lavage, was repeated on three patients receiving 60 mg prednisone per day. A decrease in the uptake of liposomes was observed after steroid treatment.     

Quantitative studies of phagocytosis by alveolar macrophages

The initial rate of phagocytosis by rabbit alveolar macrophages of paraffin oil emulsions stabilized with albumin was markedly increased by prior incubation of the emulsion with serum. The active component(s) of serum was non-dialyzable and heat-labile and was absent from zymosan-treated serum. Magnesium and calcium were both required for the maximal rate of phagocytosis. At 4 °C or in the presence of 1 mM N-ethylmaleimide, the rate of phagocytosis was less than 2% of the control (37° C) rate. The initial rates of phagocytosis of this emulsion by alveolar macrophages from rabbits injected with Freund's adjuvant were not demonstrably different from those observed with macrophages from normal rabbits. Per of mg of cell protein, polymorphonuclear leukocytes ingested serum-treated emulsion more rapidly than did macrophages, but per cell the rates were not different.     

Leukotriene B4 biosynthesis by alveolar macrophages

Resting alveolar macrophages in culture synthesized small amount of leukotriene B₄. This synthesis was increased 2.5 fold following phagocytic stimulation by zymosan, and was increased 12.6 fold after stimulation with calcium and calcium ionophore A23187. The leukotriene B₄ synthesis could be completely inhibited by nordihydroguaiaretic acid (10^?5M). Phorbol myristate acetate, a membrane perturbant, has no effect on leukotriene B₄ production by macrophages.     

Tartrate-resistant acid phosphatase in human alveolar macrophages

Tartrate-resistant acid phosphatase has been extracted from human alveolar macrophages, in which its specific activity is 10-fold that in whole lung. The apparent identity of the alveolar macrophage isoenzyme with that associated with osteoclasts suggests that both types of cell belong to the mononuclear phagocyte system. Within this system, expression of tartrate-resistant acid phosphatase appears to accompany certain kinds of differentiation.     

Collagenase from rabbit pulmonary alveolar macrophages.

Rabbit pulmonary alveolar macrophages produce a collagenase which lyses labeled collagen gels, specifically cleaves collagen types I, II and III, is inhibited by ethylenediaminetetraacetate, cysteine, dithiothreitol and serum but is not inhibited by a serine protease inhibitor. Alveolar macrophage collagenase activity can be enhanced by $\text{in vivo}$ BCG activation, $\text{in vitro}$ latex, silica or mycobacterium activation and by $\text{in vitro}$ uncovering of latent enzymatic activity with trypsin treatment. The production of collagenase by unactivated alveolar macrophages and the presence of “latent” collagenase in culture media of alveolar macrophages are examples of significant differences between alveolar and peritoneal macrophages.