Glucocorticoids mediate macrophage dysfunction in protein calorie malnutrition

Background In hospitalized patients protein calorie malnutrition substantially increases the incidence of infection and death. Protein calorie malnutrition results in significant macrophage dysfunction. Whether a primary nutrient deficit or elevated glucocorticoids levels mediate this dysfunction is...

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Bibliographic Details
Published in:Surgery 1995-08, Vol.118 (2), p.130-137
Main Authors: Hill, Arnold D.K., Naama, Hassan A., Gallagher, Hubert J., Shou, Jian, Calvano, Steven E., Daly, John m.
Format: Article
Language:English
Subjects:
Animal Nutritional Physiological Phenomena
Animals
Body Weight
Corticosterone - blood
Female
Glucocorticoids - physiology
Interleukin-6 - biosynthesis
Macrophages - physiology
Mice
Mice, Inbred Strains
Protein-Energy Malnutrition - pathology
Protein-Energy Malnutrition - physiopathology
Serum Albumin - analysis
Superoxides - metabolism
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Summary:Background In hospitalized patients protein calorie malnutrition substantially increases the incidence of infection and death. Protein calorie malnutrition results in significant macrophage dysfunction. Whether a primary nutrient deficit or elevated glucocorticoids levels mediate this dysfunction is unclear. The aim of this study was to evaluate the neuroendocrine response to protein calorie malnutrition and its effects on macrophage function. Methods By use of a murine model of protein calorie malnutrition, mice were randomized to (1) a standard 24% casein diet (control), (2) protein-free diet (PED), (3) PFD in adrenalectomized mice, (4) PFD plus the glucocorticoid receptor antagonist RU486 (10 mg/kg), or (5) a standard 24% casein diet plus a 50 mg orticosterone pellet implanted subcutaneously for 7 days. Mice were killed after 7 days, and body weight and serum albumin and corticosterone levels were measured. Peritoneal macrophages were obtained, and stimulated superoxide and interleukin-6 productions were measured. Results Protein calorie malnutrition significantly impaired macrophage function and elevated serum glucocorticoid levels. Blocking the stress corticosterone response with adrenalectomy or using RU486 to block corticosterone receptors prevented the impairment of macrophage function without restoring nutritional indexes (body weight and serum albumin level). Administration of glucocorticoids via a subcutaneous pellet reproduced macrophage impairment without leading to nutritional deficits. Conclusions
ISSN:0039-6060
1532-7361
DOI:10.1016/S0039-6060(05)80315-0