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Thymulin and Inflammatory Pain: A Possible Substrate for Pge-2 Dependent Neuroimmune Loop

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Abstract

The thymic hormone thymulin is well known for its role in immunomodulation. More recent evidence, however, points towards an important role for this thymic peptide as a signaling molecule between the immune, endocrine and the nervous system. In this review, we present the recent findings of investigations which demonstrate that thymulin injections in low concentration result in hyperalgesia accompanied with an increase in the concentration of several proinflammatory mediators. Moreover, the use of specific antagonists and antisera to the various mediators indicated a role for each one of them, the most important being PGE2. Further proof for thymulin acting on the nervous system is presented by the finding that this peptide can lead to increased fos-like immunoreactivity in the dorsal horn which can be reversed by meloxicam and morphine and the importance of capsaicin sensitive primary afferent fibers in mediating the hyperalgesic action of thymulin is emphasized.

The findings presented in this report allow us to conclude that thymulin can act directly on the afferent nerve terminals, through PGE2 mechanisms, thus forming a neuroimmune loop involving capsaicin sensitive primary afferent fibers.

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Safieh-Garabedian, B., Kanaan, S.A., Jabbur, S.J., Atweh, S.F., Saadé, N.E. (2000). Thymulin and Inflammatory Pain: A Possible Substrate for Pge-2 Dependent Neuroimmune Loop. In: Saadé, N.E., Apkarian, A.V., Jabbur, S.J. (eds) Pain and Neuroimmune Interactions. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4225-4_11

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  • DOI: https://doi.org/10.1007/978-1-4615-4225-4_11

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-6897-7

  • Online ISBN: 978-1-4615-4225-4

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