1995
DOI: 10.1016/s0039-6060(05)80315-0
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Glucocorticoids mediate macrophage dysfunction in protein calorie malnutrition*

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Cited by 28 publications
(15 citation statements)
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“…Corticosteroids are known to suppress the phagocytic capacity of both macrophages and polymorphonuclear cells [13]. Moreover, Hill et al [14] succeeded in preventing the stimulated superoxide and IL-6 production by peritoneal macrophages of malnourished mice blocking the stress corticosterone response by adrenalectomy.…”
Section: Discussionmentioning
confidence: 99%
“…Corticosteroids are known to suppress the phagocytic capacity of both macrophages and polymorphonuclear cells [13]. Moreover, Hill et al [14] succeeded in preventing the stimulated superoxide and IL-6 production by peritoneal macrophages of malnourished mice blocking the stress corticosterone response by adrenalectomy.…”
Section: Discussionmentioning
confidence: 99%
“…Glucocorticoids may control inflammation by inhibiting many aspects of the inflammatory process via an increase in the transcription of anti-inflammatory genes and a decrease in the transcription of inflammatory genes [147,149,150] .…”
Section: Leptin and Glucocorticoids In Malnutritionmentioning
confidence: 99%
“…Previous studies have identified the glucocorticoid response as an important mediator of the effects of PEM in a murine model; however, blockade of the glucocorticoid response only partially reverses PEMrelated host impairment. 1 Other factors, therefore, must contribute to the multifold effects of protein deprivation. Given that leptin is a regulator of food intake and body mass, and has hormone-like activity in the HPA, 15,16 we hypothesized that serum leptin levels are altered in PEM and that the glucocorticoid response may play a role in regulating these levels.…”
Section: As Recorded Inmentioning
confidence: 99%
“…1 In hospitalized patients, the persistent weight loss of PEM is associated with altered immune functions, leading to increased morbidity and mortality that is manifested by delayed wound healing and increased infectious complications. 1 Because hospitalized patients frequently have important comorbidities such as age, injury, and use of immunosuppressive agents, it is difficult to differentiate the independent effect of PEM in this group. 2,3 Animal models of PEM are useful to dissect the physiologic dysfunction associated with PEM. Work in this laboratory has previously shown in a murine model that a protein-free diet for 7 days significantly increases serum corticosterone, the major stress-induced murine glucocorticoid.…”
mentioning
confidence: 99%
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