Endocrine Abstracts (2004) 7 P214

Lipopolysaccharide (LPS) stimulates cortisol secretion via toll-like receptors and COX-2 activation

K Vakharia, D Renshaw & JP Hinson


Department of Endocrinology, Barts and the London, Queen Mary, University of London, UK.


Previous data from this laboratory has shown that lipopolysaccharide (LPS) is a direct stimulant of adrenal cortisol secretion. The present study was designed to determine the mechanism of this effect.

The human adrenocortical H295R cell line was used in these studies. Cells were incubated in the presence of varying concentrations of LPS (10 to 1000ng/ml) for periods up to 24 hours. PGE2 and cortisol were measured by RIA. Indomethacin and the specific COX-1 inhibitor, SC580 , and the COX-2 inhibitor, NS398 were used in the presence and absence of LPS. Forskolin was used as a positive control for cortisol secretion in these studies. The presence of message encoding Toll-like receptors 2 and 4 were confirmed by PCR.

LPS caused a time-dependent and highly significant increase in both cortisol and PGE2 release by H295R cells. Forskolin significantly stimulated cortisol, but not prostaglandin release. The effects of LPS were completely abolished by indomethacin and by NS398, the COX-2 inhibitor, but not significantly altered by the COX-1 inhibitor. Neither basal nor forskolin-stimulated cortisol secretion was altered in the presence of these inhibitors.

These data suggest that LPS stimulates cortisol secretion by a mechanism involving COX-2 and probably the toll-like receptors.

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