Can nerve damage disrupt neuroendocrine immune homeostasis?
Rook GA; Lightman SL; Heijnen CJ Dept Medical Microbiology, Windeyer Institute of Medical Sciences, Royal Free and University College Medical School, 46 Cleveland Street, W1P 6DB, London, UK. g.rook@ucl.ac.uk The crucial clinical problem in leprosy is the occurrence of acute inflammatory episodes that lead to nerve damage, even after the infecting organisms have been killed by antibiotics. We suggest that the instability of these inflammatory sites is attributable to a disturbance of the role that nerves play in the regulation of inflammation. The destruction of sensory C fibers and sympathetic innervation will remove anti-inflammatory feedback circuits. Moreover, diminishing levels of neuropeptides and changes in the cytokine profile will affect the cortisol-sensitivity of infiltrating T cells, and modulate the cortisol-cortisone shuttle so that the inflammatory site becomes resistant to physiological levels of anti-inflammatory adrenocortical steroids.
