FIGURE 1.

The figure shows a bi-phasic model of GC regulation of in vivo defense mechanisms, including innate immune inflammation. According to this model, basal concentrations of cortisol are not anti-inflammatory but exert a supportive (permissive) action on various defense mechanisms. As cortisol concentrations increase to those associated with systemic stress or pharmacological administration of cortisol, a bi-phasic relationship is observed, especially when there is a time delay between the increase in cortisol concentration and the inflammatory stimulus.