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

79 Citations (Scopus)

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
StatePublished - 1989
Externally publishedYes

Fingerprint

Neurogenic Inflammation
Neprilysin
Substance P
Respiratory Tract Infections
Trachea
Inflammation
Rat Coronavirus
Peptides
Peptide Hydrolases
Mycoplasma pulmonis
Human parainfluenza virus 1
Bronchoconstrictor Agents
Tachykinin Receptors
Bronchitis
Virus Diseases
Neuropeptides
Cough
Cystic Fibrosis
Respiratory System
Edema

ASJC Scopus subject areas

  • Endocrinology
  • Physiology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

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.

Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections. / Borson, D. B.; Brokaw, J. J.; Sekizawa, K.; McDonald, D. M.; Nadel, J. A.

In: Journal of Applied Physiology, Vol. 66, No. 6, 1989, p. 2653-2658.

Research output: Contribution to journalArticle

Borson, DB, Brokaw, JJ, Sekizawa, K, McDonald, DM & Nadel, JA 1989, 'Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections', Journal of Applied Physiology, vol. 66, no. 6, pp. 2653-2658.
Borson DB, Brokaw JJ, Sekizawa K, McDonald DM, Nadel JA. Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections. Journal of Applied Physiology. 1989;66(6):2653-2658.
Borson, D. B. ; Brokaw, J. J. ; Sekizawa, K. ; McDonald, D. M. ; Nadel, J. A. / Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections. In: Journal of Applied Physiology. 1989 ; Vol. 66, No. 6. pp. 2653-2658.
@article{964bb73bb4aa4f2c967e1b90e56c762e,
title = "Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections",
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.",
author = "Borson, {D. B.} and Brokaw, {J. J.} and K. Sekizawa and McDonald, {D. M.} and Nadel, {J. A.}",
year = "1989",
language = "English (US)",
volume = "66",
pages = "2653--2658",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "6",

}

TY - JOUR

T1 - Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections

AU - Borson, D. B.

AU - Brokaw, J. J.

AU - Sekizawa, K.

AU - McDonald, D. M.

AU - Nadel, J. A.

PY - 1989

Y1 - 1989

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0024311370&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024311370&partnerID=8YFLogxK

M3 - Article

C2 - 2545662

AN - SCOPUS:0024311370

VL - 66

SP - 2653

EP - 2658

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 6

ER -