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Catestatin (CST) is a bioactive cleavage product of the neuroendocrine prohormone chromogranin A (CgA). Recent findings show that CST can exert anti-inflammatory and antiadrenergic effects by suppressing the inflammatory actions of mammalian macrophages. However, recent findings also suggest that macrophages themselves are major CST producers. Here, we hypothesize that macrophages produce CST in an inflammation-dependent manner and thereby might self-regulate inflammation in an autocrine fashion. CST is associated with pathological conditions hallmarked by chronic inflammation, including autoimmune, cardiovascular, and metabolic disorders. Since intraperitoneal injection of CST in mouse models of diabetes and inflammatory bowel disease has been reported to be beneficial for mitigating disease, we posit that CST should be further investigated as a candidate target for treating certain inflammatory diseases. Catestatin (CST), a 21-amino acid peptide derived from proteolytic cleavage of the prohormone chromogranin A, has been reported to have anti-inflammatory and antiadrenergic functions in mice. CST is thought to be mainly co-released with catecholamines by neuroendocrine cells. Recent studies suggest that macrophages are also a source of CST and that the anti-inflammatory effects of CST might be attributable to CST produced by macrophages, at least in mice. We propose that CST produced by macrophages might suppress neuronal and neuroendocrine activity, in an inflammation-dependent manner. [ABSTRACT FROM AUTHOR]