Lipopolysaccharide enhances neurogenic plasma exudation in guinea-pig airways

H. P. Kuo, K. H. Hwang, H. C. Lin, C. H. Wang, C. Y. Liu, L. C. Lu

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

1. Lipopolysaccharide (LPS) is implicated in many pulmonary and airway inflammatory diseases. Tachykinins released from nerve endings increase vascular permeability. In this study, we have assessed the enhancement by LPS of tachykinin-mediated plasma exudation in guinea-pig airways, and examined the role of oxidants as well as leukocyte adherence. 2. LPS (100 μg kg-1, i.v.) was administered 0-3 h before bilateral electrical stimulation of the cervical vagus nerves in animals anaesthetized with urethane and ventilated. Vagal stimulation increased vascular permeability in the airways. LPS enhanced the vagally-mediated plasma exudation with the peak effect at 1 h after LPS administration. LPS alone induced no significant plasma exudation. LPS also enhanced exogenous substance P (10-8 mol kg-1, i.v.)-induced plasma exudation. 3. The NK-1 receptor antagonist L-732,138 abolished vagally-induced plasma exudation and significantly inhibited the enhancement by LPS. Pretreatment with superoxide dismutase (SOD, 5000 U kg-1, i.p.) did not affect the vagally-induced plasma exudation, but inhibited the LPS-enhanced neurogenic plasma leakage. The LPS-enhanced vagally-induced plasma exudation was not completely inhibited by either L-732,138 or SOD pretreatment alone, but was blocked by the combination of both pretreatments. 4. Neutrophil depletion by cyclophosphamide alone did not influence vagally-induced plasma exudation, but significantly inhibited the LPS-enhanced response. 5. In conclusion, we have demonstrated LPS enhanced neurogenic plasma exudation by augmenting the response to tachykinins, partly through NK-1 receptors, to directly increase vascular permeability or to enhance leukocyte adhesion-mediated endothelial cell injury. Tachykinins released from nerve endings may contribute to endotoxin-related airway inflammatory responses.

Original languageEnglish
Pages (from-to)711-716
Number of pages6
JournalBritish Journal of Pharmacology
Volume125
Issue number4
DOIs
Publication statusPublished - Nov 3 1998
Externally publishedYes

Fingerprint

Lipopolysaccharides
Guinea Pigs
Tachykinins
3,5-bis(trifluoromethyl)benzyl N-acetyltryptophan
Capillary Permeability
Neurokinin-1 Receptors
Nerve Endings
Leukocytes
Vagus Nerve
Urethane
Substance P
Oxidants
Endotoxins
Cyclophosphamide
Electric Stimulation
Superoxide Dismutase
Neutrophils
Endothelial Cells
Lung
Wounds and Injuries

Keywords

  • Lipopolysaccharide
  • Neutrophils
  • Oxidants
  • Respiratory system
  • Tachykinin
  • Vascular permeability

ASJC Scopus subject areas

  • Pharmacology

Cite this

Lipopolysaccharide enhances neurogenic plasma exudation in guinea-pig airways. / Kuo, H. P.; Hwang, K. H.; Lin, H. C.; Wang, C. H.; Liu, C. Y.; Lu, L. C.

In: British Journal of Pharmacology, Vol. 125, No. 4, 03.11.1998, p. 711-716.

Research output: Contribution to journalArticle

Kuo, H. P. ; Hwang, K. H. ; Lin, H. C. ; Wang, C. H. ; Liu, C. Y. ; Lu, L. C. / Lipopolysaccharide enhances neurogenic plasma exudation in guinea-pig airways. In: British Journal of Pharmacology. 1998 ; Vol. 125, No. 4. pp. 711-716.
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AU - Liu, C. Y.

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N2 - 1. Lipopolysaccharide (LPS) is implicated in many pulmonary and airway inflammatory diseases. Tachykinins released from nerve endings increase vascular permeability. In this study, we have assessed the enhancement by LPS of tachykinin-mediated plasma exudation in guinea-pig airways, and examined the role of oxidants as well as leukocyte adherence. 2. LPS (100 μg kg-1, i.v.) was administered 0-3 h before bilateral electrical stimulation of the cervical vagus nerves in animals anaesthetized with urethane and ventilated. Vagal stimulation increased vascular permeability in the airways. LPS enhanced the vagally-mediated plasma exudation with the peak effect at 1 h after LPS administration. LPS alone induced no significant plasma exudation. LPS also enhanced exogenous substance P (10-8 mol kg-1, i.v.)-induced plasma exudation. 3. The NK-1 receptor antagonist L-732,138 abolished vagally-induced plasma exudation and significantly inhibited the enhancement by LPS. Pretreatment with superoxide dismutase (SOD, 5000 U kg-1, i.p.) did not affect the vagally-induced plasma exudation, but inhibited the LPS-enhanced neurogenic plasma leakage. The LPS-enhanced vagally-induced plasma exudation was not completely inhibited by either L-732,138 or SOD pretreatment alone, but was blocked by the combination of both pretreatments. 4. Neutrophil depletion by cyclophosphamide alone did not influence vagally-induced plasma exudation, but significantly inhibited the LPS-enhanced response. 5. In conclusion, we have demonstrated LPS enhanced neurogenic plasma exudation by augmenting the response to tachykinins, partly through NK-1 receptors, to directly increase vascular permeability or to enhance leukocyte adhesion-mediated endothelial cell injury. Tachykinins released from nerve endings may contribute to endotoxin-related airway inflammatory responses.

AB - 1. Lipopolysaccharide (LPS) is implicated in many pulmonary and airway inflammatory diseases. Tachykinins released from nerve endings increase vascular permeability. In this study, we have assessed the enhancement by LPS of tachykinin-mediated plasma exudation in guinea-pig airways, and examined the role of oxidants as well as leukocyte adherence. 2. LPS (100 μg kg-1, i.v.) was administered 0-3 h before bilateral electrical stimulation of the cervical vagus nerves in animals anaesthetized with urethane and ventilated. Vagal stimulation increased vascular permeability in the airways. LPS enhanced the vagally-mediated plasma exudation with the peak effect at 1 h after LPS administration. LPS alone induced no significant plasma exudation. LPS also enhanced exogenous substance P (10-8 mol kg-1, i.v.)-induced plasma exudation. 3. The NK-1 receptor antagonist L-732,138 abolished vagally-induced plasma exudation and significantly inhibited the enhancement by LPS. Pretreatment with superoxide dismutase (SOD, 5000 U kg-1, i.p.) did not affect the vagally-induced plasma exudation, but inhibited the LPS-enhanced neurogenic plasma leakage. The LPS-enhanced vagally-induced plasma exudation was not completely inhibited by either L-732,138 or SOD pretreatment alone, but was blocked by the combination of both pretreatments. 4. Neutrophil depletion by cyclophosphamide alone did not influence vagally-induced plasma exudation, but significantly inhibited the LPS-enhanced response. 5. In conclusion, we have demonstrated LPS enhanced neurogenic plasma exudation by augmenting the response to tachykinins, partly through NK-1 receptors, to directly increase vascular permeability or to enhance leukocyte adhesion-mediated endothelial cell injury. Tachykinins released from nerve endings may contribute to endotoxin-related airway inflammatory responses.

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KW - Tachykinin

KW - Vascular permeability

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