Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections

D. B. Borson, J. J. Brokaw, K. Sekizawa, D. M. McDonald, J. A. Nadel

Research output: Contribution to journalArticle

80 Scopus citations

Abstract

Neuropeptides such as substance P are implicated in inflammation mediated by sensory nerves (neurogenic inflammation), but the roles in disease of these peptides and the peptidases that degrade them are not understood. It is well established that inflammation is a prominent feature of several airway diseases, including viral infections, asthma, bronchitis, and cystic fibrosis. These diseases are characterized by cough, airway edema, and abnormal secretory and bronchoconstrictor responses, all of which can be elicited by substance P. The effects of substance P and other peptides that may be involved in inflammation are decreased by endogenous neutral endopeptidase (NEP; also called enkephalinase, EC 3.4.24.11), which is a peptidase that degrades substance P and other peptides. In the present study, we report that rats with histories of infections caused by common respiratory tract pathogens (parainfluenza virus type 1, rat coronavirus, and Mycoplasma pulmonis) not only have greater susceptibility to neurogenic inflammatory responses than do pathogen-free rats but also have a lower activity of NEP in the trachea. This reduction in NEP activity may cause the increased susceptibility to neurogenic inflammation by allowing higher concentrations of substance P to reach tachykinin receptors in the trachea. Thus decreased NEP activity may exacerbate some of the pathological responses in animals with respiratory tract infections.

Original languageEnglish (US)
Pages (from-to)2653-2658
Number of pages6
JournalJournal of Applied Physiology
Volume66
Issue number6
DOIs
StatePublished - 1989

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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    Borson, D. B., Brokaw, J. J., Sekizawa, K., McDonald, D. M., & Nadel, J. A. (1989). Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections. Journal of Applied Physiology, 66(6), 2653-2658. https://doi.org/10.1152/jappl.1989.66.6.2653