Retinol Inhibition of in Vitro Human Neutrophil Superoxide Anion Release

Sharma, Anupama; Lewandoski, June R.; Zimmerman, Frederick J.

doi:10.1203/00006450-199006000-00007

Cited by 16 publications

(5 citation statements)

References 16 publications

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“…Both tumour necrosis factor α and NO were higher in our study in the VAD group; these inflammatory markers increased when insufficient amounts of VA were available. These findings are in agreement with those of previous studies that have demonstrated an anti-inflammatory effect of VA and an increase in the inflammatory process during VAD (Sharma et al 1990;Wiedermann et al 1996). Our data are also consistent with those from a human study documenting an increased risk for chronic obstructive lung disease with decreased VA intake and an inverse relationship between plasma retinol status and the extent of airway obstruction assessed by forced expiratory volume (Morabia et al 1990).…”

Section: The Respiratory Tractsupporting

confidence: 93%

“…VA supplementation could decrease an inflammatory response when rats are administered monocrotaline, a proinflammatory pneumotoxin (Swamidas et al 1999). Furthermore, the role of VA in preventing inflammation is related to its interaction with leucocytes, particularly neutrophils, as VA reduces neutrophil superoxide production (Sharma et al 1990) and VAD increases circulating leucocytes (Wiedermann et al 1996). VAD could occur as a result of the increased proliferation during tissue repair and could accelerate the ongoing inflammation.…”

Section: The Respiratory Tractmentioning

confidence: 99%

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Vitamin A as an anti-inflammatory agent

Reifen

2002

Proc. Nutr. Soc.

111

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Vitamin A is necessary for normal differentiation of epithelial tissues, the visual process and reproduction, and is vital for the optimal maintenance and functioning of the innate and adaptive immune system. Vitamin A deficiency is one of the most profuse nutritional deficiencies worldwide. It is associated with increased susceptibility to infectious diseases in both man and animal models. Vitamin A also has a role as an anti-inflammatory agent. Supplementation with vitamin A has been found to be beneficial in a number of inflammatory conditions, including skin disorders such as acne vulgaris, broncho-pulmonary dysplasia and some forms of precancerous and cancer states. The present review suggests that vitamin A deficiency induces inflammation and aggravates existing inflammatory states. Supplementation with vitamin A in selected cases could ameliorate inflammation. The two main mechanisms which appear to be involved in the prevention of disease are the effects of vitamin A on the immune system and the effect on epithelial integrity.

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Section: The Respiratory Tractsupporting

confidence: 93%

Section: The Respiratory Tractmentioning

confidence: 99%

Vitamin A as an anti-inflammatory agent

Reifen

2002

Proc. Nutr. Soc.

111

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“…Accumulated neutrophils can injure vessels by producing ROS, inflammatory cytokines, and elastase. Previous studies have suggested that neutrophils have important roles in the pathogenesis of vasculitis and that retinoid directly inhibits the production of superoxide anion and release of proteolytic enzymes by human and rat neutrophils (14, 15, 36). However, the effects on neutrophils vary among the different retinoids (15).…”

Section: Discussionmentioning

confidence: 99%

Am80, a retinoic acid receptor agonist, ameliorates murine vasculitis through the suppression of neutrophil migration and activation

Miyabe¹,

Miyabe²,

Miura³

et al. 2013

Arthritis & Rheumatism

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Objective. Vasculitis is characterized by leukocyte infiltration in the vessel walls, with destructive damage to mural structures. Retinoids are compounds that bind to retinoic acid receptors and exert biologic activities similar to those of vitamin A, including modulatory effects on cell proliferation and differentiation. This study was undertaken to examine the therapeutic effects of a synthetic retinoid, Am80, in a murine model of vasculitis induced by Candida albicans water-soluble fraction (CAWS). Vasculitis is defined by the presence of inflammatory leukocytes in vessel walls, with destructive damage to mural structures. Antineutrophil cytoplasmic antibodies are often detected in certain types of vasculitis, such as microscopic polyangiitis. The affected vessels vary in size, type, and location according to the type of vasculitic disease (1). Although the exact mechanisms

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“…These findings parallel the results of the uptake studies. Although there have been several reports which suggest that retinoids inhibit superoxide anion release in neutrophils (Sharma et al, 1990;Eisenstat et al, 1982;Shinwell et al, 1988), differences in incubation period, type of cell, and concentration of retinoids may explain these differences.…”

Section: Discussionmentioning

confidence: 99%

Retinoids upregulate phagocytosis by human dermal microvascular endothelial cells

Vora

Karasek

1994

Journal Cellular Physiology

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Animals fed a diet deficient in vitamin A show severe physiological changes that often result in death. At the cellular level, retinoids have been shown to induce differentiation of cells derived from a wide spectrum of tissues, including the vasculature. To understand further the mechanisms for these events, we studied the effects of 13-cis-retinoic acid, all-trans-retinoic acid, all-trans-retinol, and all-trans-retinol acetate on human dermal microvascular endothelial cells (HDMEC). Concentrations of retinoids in the physiological range from 0 to 1 microM were used in our experiments. These concentrations were nontoxic to HDMEC. Here we report that in addition to the known effect of retinoids on keratinocytes and sebacytes, retinoids induced morphological and functional changes in HDMEC that gave these cells macrophage like characteristics. 13-Cis-retinoic acid and all-trans-RA induced HDMEC to phagocytize and to increase the production of hydrogen peroxide and superoxide anion. These two retinoids also changed the morphology of endothelial cells from typical small compact cuboidal epithelioid cells to cells with larger cytoplasm and indistinct cell membranes. The retinoid-stimulated HDMEC deposited increased amounts of extracellular matrix. All-trans-retinol and all-trans-retinol acetate did not significantly affect HDMEC in all parameters tested. The induction of these properties provides a new model with which to study how retinoids regulate gene expression using a normal, nontransformed cell line.

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Retinol Inhibition of in Vitro Human Neutrophil Superoxide Anion Release

Cited by 16 publications

References 16 publications

Vitamin A as an anti-inflammatory agent

Vitamin A as an anti-inflammatory agent

Am80, a retinoic acid receptor agonist, ameliorates murine vasculitis through the suppression of neutrophil migration and activation

Retinoids upregulate phagocytosis by human dermal microvascular endothelial cells

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