Thymulin is a thymic hormone with known immunomodulatory activities. Recent evidence has indicated a signaling role for this peptide in the interaction between the immune, endocrine and the nervous system. In this report, we review recent experimental findings on the analgesic actions of thymulin (high doses) in rats with endotoxin-induced localized inflammation and the hyperalgesic actions (low doses) of this peptide in intact animals. These actions involve both proinflammatory cytokines and PGE₂. The possibility of a dual role played by thymulin as a hormone that might also involve a direct effect on the nervous system is discussed.

Thymulin is a neuroendocrine hormone with immunoregulatory actions. Originally known as 'serum thymic factor' (FTS), thymulin binds to a carrier protein and zinc (Zn2+) to exert its biologic properties. Thymulin, albeit an essential hormone for the T lymphocyte differentiation and the normalization of the ratio of T-helper cells to suppressor cells, accumulating evidence suggests its involvement in inflammations of various etiologies. Recently, thymulin has been shown to have anti-nociceptive effects in hyperalgesia and in pain of neurogenic origin, ostensibly through action on sensory afferents and the release of anti-inflammatory mediators. Given its anti-inflammatory potential, thymulin downregulates the release of inflammatory mediators, such as cytokines and chemokines, upregulates anti-inflammatory factors, such as interleukin (IL)-10, and exerts molecular control via the regulation of transcription factors and mediators. Recent evidence tends to indicate that thymulin can be a therapeutic agent in many inflammatory diseases and in pathological conditions affecting the peripheral and/or the central nervous system. This review discusses current concepts in the antiinflammatory actions of thymulin and correlates this activity with an emerging theme for therapeutic treatment.

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