Maturational changes in superoxide anion production of rabbit alveolar macrophages

Kojima, Tkakatsugu; Hattori, Kousuke; Fujiwara, Toru; Hirata, Yukio; Kobayashi, Yohnosuke

doi:10.1016/0024-3205(94)00536-2

Cited by 6 publications

(4 citation statements)

References 15 publications

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“…Some studies have reported that the ligation of endothelin receptors on macrophages can result in increased cytokine production and the increased production of reactive oxygen species (Haller et al, 1991; Kojima et al, 1994; Ruetten and Thiemermann, 1997; Speciale et al, 1998). To fully characterize the expression of the endothelin axis by DH82 cells, we performed reverse-transcriptase PCR (RT-PCR) on cDNAs derived from DH82 cells cultured in the absence or presence of LPS.…”

Section: Resultsmentioning

confidence: 99%

Endothelin-1 production by the canine macrophage cell line DH82: Enhanced production in response to microbial challenge

Divino

Chawla

Silva

et al. 2010

Veterinary Immunology and Immunopathology

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Endothelin-1 (ET-1) is a potent vasoconstrictive peptide which plays an important role in regulating mammalian cardiovascular development and homeostasis. Originally identified as a factor released by vascular endothelial cells, ET-1 is now recognized as a product of numerous cells and tissues with demonstrated involvement in an array of physiological and pathological processes. An area of great interest is the production of ET-1 by mononuclear cells (monocytes and macrophages) and its role in inflammation. We report that the canine macrophage cell line, DH82, constitutively secretes both ET-1 and its biologically inactive precursor big ET-1. The production of both peptides was increased following stimulation with lipopolysaccharide (endotoxin) from gram-negative bacteria. ET-1 production was also increased in response to stimulation with intact and viable gram-positive and gram-negative bacteria. In addition to producing ET-1, DH82 cells express transcripts encoding two receptors for the ET-1 peptide (ET A and ET B receptors) and an enzyme involved in the conversion of big ET-1 to ET-1. The constitutive secretion of ET-1 and the expression of ET A and ET B receptors may be related to the malignant origin of this cell line. Our results are the first report of ET-1 production by a canine cell line and provide the basis for further investigation into the role of ET-1 during infection and inflammation.

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Section: Resultsmentioning

confidence: 99%

Endothelin-1 production by the canine macrophage cell line DH82: Enhanced production in response to microbial challenge

Divino

Chawla

Silva

et al. 2010

Veterinary Immunology and Immunopathology

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“…43 Moreover, endothelin may increase oxidative stress by increasing oxygen free-radical formation from macrophages. 19 Thus, oxida- tive stress promotes an atherogenic environment of increased endothelin-1, decreased NO, and increased lipid peroxidation. In addition to the atherosclerotic effects, oxidative stress can also alter vascular tone.…”

Section: Discussionmentioning

confidence: 99%

“…17,18 Additionally, endothelin-1 may increase oxidative stress by increasing oxygen free-radical formation from macrophages. 19 Therefore, the current investigation was undertaken with the objectives to determine (1) whether chronic endothelin receptor antagonism in hypercholesterolemia preserves coronary epicardial and arteriolar endothelial function in vitro, (2) whether chronic endothelin receptor antagonism attenuates the reduction in plasma total oxidized products of NO (NO x ) and coronary endothelial NOS immunostaining associated with hypercholesterolemia, and (3) whether chronic endothelin receptor antagonism decreases plasma F 2 -isoprostane levels, an in vivo marker of oxidative stress, in experimental hypercholesterolemia.…”

mentioning

confidence: 99%

Coronary Endothelial Function Is Preserved With Chronic Endothelin Receptor Antagonism in Experimental Hypercholesterolemia In Vitro

Best

Lerman

Romero

et al. 1999

ATVB

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Abstract-Hypercholesterolemia is associated with increased circulating and tissue endothelin-1 immunoreactivity, decreased nitric oxide (NO) activity, and altered endothelial function. We tested the hypothesis that chronic endothelin receptor antagonism preserves endothelial function and increases NO in experimental porcine hypercholesterolemia. Pigs were randomized to 3 groups: Group 1, a 2% high-cholesterol (HC) diet alone (nϭ7); group 2, RO-48-5695, a combined endothelin receptor antagonist, and an HC diet (nϭ8); and group 3, ABT-627, a selective endothelin-A receptor antagonist, and an HC diet (nϭ8). Coronary epicardial and arteriolar endothelial function was determined by a dose-response relaxation to bradykinin (10 Ϫ11 to 10 Ϫ6 mol/L), in all groups and in pigs maintained on a normal diet. Plasma total oxidized products of NO (NO x ) were determined by chemiluminescence at baseline and after 12 weeks. Bradykinin-stimulated coronary epicardial and arteriolar relaxation in group 1 was attenuated compared with normal-diet controls. This relaxation was normalized with endothelin receptor antagonism. Plasma NO x decreased after 12 weeks in group 1 (Ϫ74.8Ϯ5.5%). This decrease was attenuated in the endothelin receptor antagonist groups (group 2, Ϫ28.2Ϯ15.0%; group 3, Ϫ38.9Ϯ20.6%). Chronic endothelin receptor antagonism preserves coronary endothelial function and increases NO in hypercholesterolemia. This study supports a role of endothelin-1 in the regulation of NO activity and suggests a possible therapeutic role for endothelin receptor antagonists in hypercholesterolemia.

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“…Age-related functional differences have been reported in macrophages recovered from different tissues and species (De La Fuente, 1985;Lavie & Gershon, 1988;Lavie et al ., 1992;Kojima et al ., 1994;Martin et al ., 1995). As phagocytosis is one of the main functions of macrophages, a decline in the phagocytic activity may be considered as one of the principal causes of defective host defence mechanisms in the alveolar space associated with aging.…”

Section: Introductionmentioning

confidence: 99%

Age‐dependent change in reactive oxygen species and nitric oxide generation by rat alveolar macrophages*

et al. 2003

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SummaryImmunosenescence is an age-associated dysregulation of the immune function, which contributes to increased susceptibility to disease in the elderly. Alveolar macrophages (AM) are known phagocytes that generate reactive oxygen species (ROS) and nitric oxide (NO), essential mediators for host defence. We studied phagocytosis, ROS and NO production in AM obtained from young, adult and senescent rats (1-2, 9-12 and 18-24 months old, respectively) after exposure to lipopolysaccharide (LPS, 0.1-10 µ µ µ µ g mL), 12-O-tetradecanoylphorbol 13-acetate (TPA, 0.1 µ µ µ µ g mL − − − − 1 ) or LPS + TPA in culture. Phagocytosis was significantly lower in control AM from adult rats than in AM from young animals. Nevertheless, AM from adult animals pretreated with LPS exhibited higher phagocytic capacity than AM from younger animals. ROS was identified by the NBT test at single cell level and quantified by automated image analysis. When TPA was added to all three populations, AM from adult and senescent animals responded more than AM from young animals. All LPS-stimulated AM produce more NO than controls. However, NO production increased three-, four-and two-fold in young, adult and senescent animals, respectively. Our results demonstrate that AM from young, adult and senescent animals display differential responsiveness to inflammatory mediators. Therefore, aging processes markedly affect AM metabolic functions and may further compromise the lung immune defence response, increasing adverse long-term health effects.

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Maturational changes in superoxide anion production of rabbit alveolar macrophages

Cited by 6 publications

References 15 publications

Endothelin-1 production by the canine macrophage cell line DH82: Enhanced production in response to microbial challenge

Endothelin-1 production by the canine macrophage cell line DH82: Enhanced production in response to microbial challenge

Coronary Endothelial Function Is Preserved With Chronic Endothelin Receptor Antagonism in Experimental Hypercholesterolemia In Vitro

Age‐dependent change in reactive oxygen species and nitric oxide generation by rat alveolar macrophages*

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