Endotoxin tolerance of adrenal gland: attenuation of XXXX production in response to lipopolysaccharide and @entity4545 .

@entity1 @entity4545 @entity6306 @entity295 @entity17296 @entity1887 @entity3124 @entity2819 @entity134 @entity5343 @entity701 @entity35 @entity12288 @entity7942
OBJECTIVES: Reversible @entity1887 frequently has been diagnosed in @entity3124 @entity1 with @entity295 who have either low basal @entity701 levels or low @entity701 responses to @entity4545 (ACTH) stimulation. It is generally accepted that a phenomenon called "endotoxin tolerance" contributes to immunosuppression during @entity295 . The present study was to investigate whether endotoxin tolerance occurs in the adrenal gland, leading to @entity6306 of adrenal gland during @entity295 . DESIGN: Controlled laboratory experiment. SETTING: University research laboratory. SUBJECTS: Sprague-Dawley male @entity35 200-250 g and primary isolated adrenal @entity12288 cells. INTERVENTIONS: @entity35 received intra-arterial injection of purified lipopolysaccharide (0.5 mg/kg) through indwelling femoral arterial catheters, and 24 hrs later the adrenocortical sensitivity to exogenous ACTH (10 ng/kg) was detected. Primary @entity12288 cells were pretreated with lipopolysaccharide at 0.1-100 ng/mL or with ACTH at 0.01-10 ng/mL and then challenged, in fresh media, with 1  g/mL lipopolysaccharide or 10 ng/mL ACTH. MEASUREMENTS AND MAIN RESULTS: @entity7942 was expressed in adrenal gland and primary @entity12288 cells. Plasma @entity2819 response to ACTH was decreased in @entity35 receiving preinjection of lipopolysaccharide. Lipopolysaccharide pretreatment caused a significant decrease in @entity2819 production in response to subsequent ACTH and lipopolysaccharide stimulation in primary @entity12288 cells. @entity17296 pretreatment inhibited ACTH- and lipopolysaccharide-induced expression of @entity134 metabolizing enzymes. Lipopolysaccharide significantly decreased @entity7942 and ACTH receptor expression. CONCLUSIONS: Pre-exposure to lipopolysaccharide resulted in @entity6306 to ACTH stimulation in @entity35 . In vitro, @entity17296 pretreatment impaired @entity2819 production of @entity12288 cells in response to ACTH and lipopolysaccharide, which was associated with decreased expression of synthetic enzymes required for @entity2819 production. Our results indicate that endotoxin tolerance of adrenal gland is one of the mechanisms for @entity5343 during @entity295 .
