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Glucocorticoids mediate macrophage dysfunction in protein calorie malnutrition
A D Hill1, H A Naama, H J Gallagher
1Department of Surgery, New York Hospital/Cornell University Medical Center, New York 10021, USA.
Surgery
|August 1, 1995
Summary
Protein calorie malnutrition impairs macrophage function, increasing infection risk. Elevated corticosterone, a stress hormone, drives this dysfunction, not just nutrient deficiency. This highlights the neuroendocrine impact on immune cells.
Area of Science:
- Immunology
- Endocrinology
- Nutrition Science
Background:
- Protein calorie malnutrition (PCM) in hospitalized patients correlates with increased infection and mortality.
- PCM leads to significant macrophage dysfunction, but the mediating factors (nutrient deficit vs. glucocorticoids) remain unclear.
Purpose of the Study:
- To investigate the neuroendocrine response to PCM.
- To determine the impact of this response on macrophage function.
Main Methods:
- A murine model of PCM was used, with groups receiving different diets (control, protein-free) and interventions (adrenalectomy, glucocorticoid receptor antagonist RU486, corticosterone pellets).
- Macrophage function was assessed by measuring superoxide and interleukin-6 production.
- Serum corticosterone and albumin levels, along with body weight, were measured.
Main Results:
- PCM impaired macrophage function and elevated serum glucocorticoid levels.
- Blocking the corticosterone response (via adrenalectomy or RU486) prevented macrophage dysfunction without improving nutritional status.
- Exogenous glucocorticoid administration mimicked PCM-induced macrophage impairment.
Conclusions:
- The neuroendocrine response, specifically elevated serum corticosterone, is a key factor in macrophage dysfunction during PCM.
- Glucocorticoids, rather than solely nutrient deficiency, mediate the immune impairment seen in PCM.