Requirement of peptidergic sensory innervation for disease activity in murine models of immune hepatitis and protection by beta-adrenergic stimulation

J Neuroimmunol. 1999 May 3;96(2):131-43. doi: 10.1016/s0165-5728(99)00014-4.

Abstract

To investigate the interaction between the peripheral nervous and the immune system in vivo, we used two mouse models of T cell and TNF-alpha dependent liver injury inducible by either concanavalin A or a combination of D-galactosamine and staphylococcal enterotoxin B. Mice depleted of peptidergic sensory nerve fibres by capsaicin were protected from liver injury. Moreover, TNF-alpha production was significantly reduced. Examination of the effect of catecholamines on liver injury showed that the beta2-adrenergic agonist salbutamol prevented, whereas chemical sympathectomy by 6-hydroxydopamine, deteriorated the disease. Hence, strategies reducing the activity of peptidergic sensory nerve fibres or stimulating beta2-adrenoreceptors, may be of benefit in immune-mediated liver disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenergic beta-Agonists / pharmacology
  • Albuterol / pharmacology
  • Animals
  • Capsaicin / pharmacology
  • Catecholamines / physiology
  • Hepatitis, Animal / pathology
  • Hepatitis, Animal / physiopathology*
  • Immune System Diseases / physiopathology*
  • Liver / innervation
  • Liver / pathology
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Nerve Fibers / metabolism
  • Neurons, Afferent / drug effects
  • Neurons, Afferent / physiology*
  • Receptors, Adrenergic, beta / physiology*
  • Sympathectomy, Chemical

Substances

  • Adrenergic beta-Agonists
  • Catecholamines
  • Receptors, Adrenergic, beta
  • Albuterol
  • Capsaicin