Insufficient glucocorticoid signaling and elevated inflammation in coronary heart disease patients with comorbid depression

Depression
DOI: 10.1016/j.bbi.2015.02.002 Publication Date: 2015-02-12T19:16:54Z
ABSTRACT
Coronary heart disease (CHD) and depression are very common often co-existing disorders. In addition to psychological social morbidity, exacerbates adverse cardiac outcomes in CHD patients. Inflammation has been proposed as one of the mechanisms involved association between these two debilitating diseases. Therefore, present study aimed evaluate inflammatory responses well investigate pathophysiological underlying putative activation patients with without depression, by assessing function important biological factors regulating inflammation, hypothalamus-pituitary-adrenal (HPA) axis glucocorticoid receptor (GR). Eighty-three (n=28) (n=55) comorbid were recruited from primary care services South London. Depression status was assessed means Clinical Interview Schedule Revised for diagnosis Beck Inventory presence depressive symptoms. Serum C-reactive protein (CRP), plasma vascular endothelial growth factor (VEGF), salivary cortisol measured using commercially available ELISA kits. Gene expression GR interleukin-6 (IL-6) conducted via qPCR. sensitivity evaluated vitro isolated peripheral blood mononuclear cells dexamethasone inhibition lipopolysaccharide-stimulated IL-6 levels. levels kynurenine pathway metabolites high performance liquid chromatography. Our results show that had higher CRP, gene expression, VEGF compared non-depressed, lower saliva The depressed group also exhibited a reduction sensitivity. Finally, tryptophan significantly who showed an increased kynurenine/tryptophan ratio. conclusion, elevated inflammation context HPA hypoactivity, resistance, pathway. Reduced bioavailability attenuated responsiveness due decreased may lead insufficient signaling thus elevation
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