Dexamethasone and methylprednisolone affect rat peritoneal phagocyte chemiluminescence after administration in vivo

Røshol, Hilde; Skrede, Knut Kristian; Ærø, C. E.; Wiik, Pål

doi:10.1016/0014-2999(95)00430-s

Cited by 23 publications

(26 citation statements)

References 38 publications

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“…These results could be correlated with other studies investigating the effects of corticosteroids on bronchial responsiveness [25]. The anti-inflammatory effects of corticosteroids on ROS inhibition in various cell types are controversial [21]. In vitro studies have suggested that the anti-inflammatory action of corticosteroids depends at least partially on an interference with the formation of reactive oxygen species by phagocytes [26].…”

Section: Discussionsupporting

confidence: 73%

“…The phorbol ester PMA binds and activates protein kinase C which is then translocated to the membrane [32]. The responses to the common three stimulators used to stimulate superoxide anion production (PMA, N-formylmethionyl leucyl phenylalanine (fMLP) and opsonized zymosan) were affected similarly by corticosteroids [21]. This suggests that corticosteroids commonly affect components in the activation pathway, possibly protein kinase C or NADPH oxidase.…”

Section: Discussionmentioning

confidence: 77%

“…Ex vivo inhaled steroid treatment had no effect on superoxide anion production in human alveolar macrophages [19,20]. In contrast, a recent study showed that in vivo administration of dexamethasone or methylprednisolone led to a dose-dependent inhibition of rat peritoneal leucocyte chemiluminescence [21]. Moreover, hydrocortisone was found to inhibit superoxide anion production during an asthma attack [22].…”

mentioning

confidence: 99%

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Superoxide anion production by monocytes of corticosteroid-treated asthmatic patients

Majori

Vachier²,

Godard³

et al. 1998

Eur Respir J

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Bronchial asthma is a chronic inflammatory disease of the airways characterized by an increased recruitment of inflammatory cells, including mononuclear phagocytic cells such as monocytes [1]. The ability of these cells to generate highly reactive oxygen species (ROS), including super-oxide anion, following activation of a membraneassociated reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is an important part of the host defence system, and has also been implicated in inflammation in a variety of pulmonary diseases [2,3], including asthma [4,5]. Oxygen metabolites cause tissue injury, smooth muscle contraction, increased airway vascular permeability, and may increase airway responsiveness and release of var-ious mediators [4].In previous studies, it has been shown that alveolar macrophages [6], blood monocytes [5] and eosinophils [7] from asthmatic patients were able to produce high amounts of ROS. Alveolar macrophage activation was correlated with the severity of asthma [6]. This activation occurred immediately after antigen challenge, and the appearance of high-density macrophages which release higher amounts of superoxide anion occurred during the late airway response [8]. Several investigators have also suggested that polymorphonuclear leucocytes from asthmatic patients generated more ROS than control subjects [9,10]. This activation was correlated with the level of bronchial hyperreactivity [11].Corticosteroids are the most potent anti-inflammatory agents available for the treatment of asthma [12], but little is known about their molecular mechanism of action in improving symptoms or the way they reduce hyperresponsiveness. It has been proposed that corticosteroids inhibit the inflammatory process by redirection of lymphocyte traffic, inhibition of cytokine gene expression [13] and inhibition of the expression of adhesion molecules [14].The effect of anti-inflammatory corticosteroids on oxygen radical production by phagocytes has been less extensively studied, and the results are contradictory. In vitro studies have demonstrated an inhibitory effect of high corticosteroid concentrations on oxygen radical production in human granulocytes [15]. In contrast, dexamethasone treatment has been reported to have no effect on ROS secretion in human blood-derived macrophages [16], but have a stimulatory effect on human monocytes [17]. It has been reported that in vivo corticosterone had no effect on murine peritoneal inflammatory cells [18]. Ex vivo inhaled steroid treatment had no effect on superoxide anion production in human alveolar macrophages [19,20]. In contrast, a recent study showed that in vivo administration of dexamethasone or methylprednisolone led to a dose-dependent inhibition of rat peritoneal leucocyte chemiluminescence [21]. Moreover, hydrocortisone was found to inhibit superoxide anion production during an asthma attack [22].Superoxide anion production by monocytes of corticosteroid-treated asthmatic patients. M. Majori, I. Vachier, P. Godard, M. Farce, J. Bousquet, P. Chanez. ...

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 77%

mentioning

confidence: 99%

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Superoxide anion production by monocytes of corticosteroid-treated asthmatic patients

Majori

Vachier²,

Godard³

et al. 1998

Eur Respir J

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“…Corticosteroids produce significant inhibition of superoxide anion release by human monocytes in normal subjects [16] or asthmatic patients [17], as well as human granulocytes [18]. In vivo administration of corticosteroids leads to a dose-dependent inhibition of rat peritoneal leucocyte chemiluminescence [19]. Corticosteroids may also raise leucocyte intracellular levels of ROS scavenging enzymes, as superoxide dismutase, catalase and glutathione peroxidase [20].…”

Section: Introductionmentioning

confidence: 99%

Peripheral parameters of oxidative stress in patients with infiltrative Graves’ ophthalmopathy treated with corticosteroids

2004

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“…Further studies with synthetic glucocorticoids given to rats in vivo have confirmed and substantiated a strong negative effect on monocyte-macrophage function in nanomolar concentrations (Rashol et al, 1995). Studies of experimental inflammation in rats indicate that glucocorticoids in vivo strongly inhibit the chemotaxis of monocytes to the peritoneum but not the chemotaxis of granulocytes (Unpublished results, T. Haugedal, Norwegian Defence Research Establishment, Kjeller, Norway, 1995).…”

Section: Pälw1ikmentioning

confidence: 94%

Military Strategies for Sustainment of Nutrition and Immune Function in the Field

Poos¹,

Costello²,

Carlson-Newberry³

1999

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The serpent has been a symbol of long life, healing, and knowledge among almost all cultures and religions since the beginning of recorded history. The image adopted as a logotype by the Institute of Medicine is based on a relief carving from ancient Greece, now held by the Staatliche Museen in Berlin.Cover: Resting monocyte/macrophage being activated to produce proinflammatory cytokines which form complexes with receptor binding proteins. Adapted from COMMITTEE ON MILITARY NUTRITION RESEARCHROBERT O. NESHEIM (Chair, through June 30, 1998) (FNB), Institute of Medicine, National Academy of Sciences. Other workshops or symposia have included such topics as food components to enhance performance; nutritional needs in hot, cold, and high-altitude environments; body composition and physical performance; nutrition and physical performance; cognitive testing methodology; and fluid replacement and heat stress. These workshops form part of the response that the CMNR provides to the Commander, U. HISTORY OF THE COMMITTEEThe CMNR was established in October 1982 following a request by the Assistant Surgeon General of the Army that the Board on Military Supplies of the National Academy of Sciences set up a special committee. The purpose of this committee was to advise the U.S. Department of Defense on the need for and conduct of nutrition research and related issues. The CMNR was transferred to the FNB in 1983. The CMNR's current tasks are• to identify nutritional factors that may critically influence the physical and mental performance of military personnel under all environmental extremes,• to identify deficiencies in the existing database, • to recommend research that would remedy these deficiencies as well as approaches for studying the relationship of diet to physical and mental performance, and• to review and advise on standards for military feeding systems.Within this context, the CMNR was asked to focus on nutrient requirements for performance during operational missions rather than requirements for military personnel in garrison (the latter were judged to be not significantly different from those of the civilian population).Although the membership of the committee has changed periodically, the disciplines represented consistently have included human nutrition, nutritional biochemistry, performance physiology, food science, and psychology. For issues that require broader expertise than exists within the committee, the CMNR has convened workshops or utilized consultants. The workshops provide additional state-of-the-art scientific information and informed opinion for the consideration of the committee. COMMITTEE TASKS AND PROCEDURESThe request for this review of nutrition and immune function and its application to military operations originated with Army scientists from USARIEM and USAMRMC. In December 1995, a committee subgroup of the CMNR participated in a series of conference calls with USARIEM, USAMRMC, and other CMNR members to identify the key areas that should be reviewed and to solicit suggestions for names...

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Dexamethasone and methylprednisolone affect rat peritoneal phagocyte chemiluminescence after administration in vivo

Cited by 23 publications

References 38 publications

Superoxide anion production by monocytes of corticosteroid-treated asthmatic patients

Superoxide anion production by monocytes of corticosteroid-treated asthmatic patients

Peripheral parameters of oxidative stress in patients with infiltrative Graves’ ophthalmopathy treated with corticosteroids

Military Strategies for Sustainment of Nutrition and Immune Function in the Field

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