and innate immune-cell function. Similarly, the hypothalamic peptide β-endorphin (BEP), whose release is stimulated by CRH during HPA activation, can inhibit stress-hormone production and activate peripheral immune functions (Sarkar and Zhang 2013). All of these findings suggest that the stress–HPA axis, commonly thought to involve anti-inflammatory glucocorticoid actions, also contributes to stress–alcohol responses in the brain that can increase proinflammatory HMGB1–TLR–cytokine signaling.
