Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections.
Identifieur interne : 000D77 ( PubMed/Checkpoint ); précédent : 000D76; suivant : 000D78Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections.
Auteurs : D B Borson ; J J Brokaw ; K. Sekizawa ; D M Mcdonald ; J A NadelSource :
- Journal of applied physiology (Bethesda, Md. : 1985) [ 8750-7587 ] ; 1989.
Descripteurs français
- KwdFr :
- Animaux, Femelle, Infections de l'appareil respiratoire (enzymologie), Infections de l'appareil respiratoire (physiopathologie), Infections à Coronaviridae (enzymologie), Infections à Coronaviridae (physiopathologie), Infections à Mycoplasma (enzymologie), Infections à Mycoplasma (physiopathologie), Infections à Paramyxoviridae (enzymologie), Infections à Paramyxoviridae (physiopathologie), Néprilysine (métabolisme), Perméabilité capillaire, Rats, Trachée (enzymologie), Virus parainfluenza humain de type 1.
- MESH :
- enzymologie : Infections de l'appareil respiratoire, Infections à Coronaviridae, Infections à Mycoplasma, Infections à Paramyxoviridae, Trachée.
- métabolisme : Néprilysine.
- physiopathologie : Infections de l'appareil respiratoire, Infections à Coronaviridae, Infections à Mycoplasma, Infections à Paramyxoviridae.
- Animaux, Femelle, Perméabilité capillaire, Rats, Virus parainfluenza humain de type 1.
English descriptors
- KwdEn :
- Animals, Capillary Permeability, Coronaviridae Infections (enzymology), Coronaviridae Infections (physiopathology), Female, Mycoplasma Infections (enzymology), Mycoplasma Infections (physiopathology), Neprilysin (metabolism), Parainfluenza Virus 1, Human, Paramyxoviridae Infections (enzymology), Paramyxoviridae Infections (physiopathology), Rats, Respiratory Tract Infections (enzymology), Respiratory Tract Infections (physiopathology), Trachea (enzymology).
- MESH :
- chemical , metabolism : Neprilysin.
- enzymology : Coronaviridae Infections, Mycoplasma Infections, Paramyxoviridae Infections, Respiratory Tract Infections, Trachea.
- physiopathology : Coronaviridae Infections, Mycoplasma Infections, Paramyxoviridae Infections, Respiratory Tract Infections.
- Animals, Capillary Permeability, Female, Parainfluenza Virus 1, Human, Rats.
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 corona-virus, 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.
DOI: 10.1152/jappl.1989.66.6.2653
PubMed: 2545662
Affiliations:
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Sekizawa</name></author><author><name sortKey="Mcdonald, D M" sort="Mcdonald, D M" uniqKey="Mcdonald D" first="D M" last="Mcdonald">D M Mcdonald</name></author><author><name sortKey="Nadel, J A" sort="Nadel, J A" uniqKey="Nadel J" first="J A" last="Nadel">J A Nadel</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1989">1989</date><idno type="RBID">pubmed:2545662</idno><idno type="pmid">2545662</idno><idno type="doi">10.1152/jappl.1989.66.6.2653</idno><idno type="wicri:Area/PubMed/Corpus">000D97</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000D97</idno><idno type="wicri:Area/PubMed/Curation">000D97</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000D97</idno><idno type="wicri:Area/PubMed/Checkpoint">000D77</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000D77</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections.</title><author><name sortKey="Borson, D B" sort="Borson, D B" uniqKey="Borson D" first="D B" last="Borson">D B Borson</name><affiliation><nlm:affiliation>Cardiovascular Research Institute, University of California, San Francisco 94143-0130.</nlm:affiliation><wicri:noCountry code="subField">San Francisco 94143-0130</wicri:noCountry></affiliation></author><author><name sortKey="Brokaw, J J" sort="Brokaw, J J" uniqKey="Brokaw J" first="J J" last="Brokaw">J J Brokaw</name></author><author><name sortKey="Sekizawa, K" sort="Sekizawa, K" uniqKey="Sekizawa K" first="K" last="Sekizawa">K. 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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 corona-virus, 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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">2545662</PMID><DateCompleted><Year>1989</Year><Month>08</Month><Day>22</Day></DateCompleted><DateRevised><Year>2017</Year><Month>12</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">8750-7587</ISSN><JournalIssue CitedMedium="Print"><Volume>66</Volume><Issue>6</Issue><PubDate><Year>1989</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Journal of applied physiology (Bethesda, Md. : 1985)</Title><ISOAbbreviation>J. Appl. Physiol.</ISOAbbreviation></Journal><ArticleTitle>Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections.</ArticleTitle><Pagination><MedlinePgn>2653-8</MedlinePgn></Pagination><Abstract><AbstractText>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 corona-virus, 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. 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