01390nas a2200253 4500000000100000008004100001260001300042653002800055653001600083653001100099653001700110653001200127653001700139653001900156653002700175100001100202700001500213700001400228245009200242300001000334490000700344520077100351022001401122 2002 d c2002 Jan10aAdrenal Cortex Hormones10aHomeostasis10aHumans10aInflammation10aleprosy10aNerve Fibers10aNervous System10aNeurosecretory Systems1 aRook G1 aLightman S1 aHeijnen C00aCan nerve damage disrupt neuroendocrine immune homeostasis? Leprosy as a case in point. a18-220 v233 a

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.

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