In vitro red tide toxin effects on human bronchial smooth muscle

Terufumi Shimoda, Joseph Krzanowski, Robert Nelson, Dean F. Martin, James Polson, Robert Duncan, Richard Lockey

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Airborne Ptychodiscus brevis toxin (PBTX), produced by Ptychodiscus brevis (Florida red tide), induces cough, rhinorrhea, watery eyes, and sneezing in normal individuals and wheezing in subjects with asthma. The mechanism of PBTX-induced contractile response has been investigated by the authors in vitro in dog and rat tissue. PBTX stimulates neuronal sodium channels, resulting in activation of autonomic cholinergic and adrenergic nerve endings in canine upper and lower airway smooth muscle and in rat vas deferens, respectively. This article concerns the investigation of the effect and mechanism of action of PBTX on human airways in order to determine the unique role of the toxin in the pathogenesis of asthma. PBTX elicited contractions of isolated human airway smooth muscle with a threshold concentration of 0.1 μg/ml, a peak response at 12.0 μg/ml, and an effective concentration for 50% of 1.24 μg/ml, very similar to values obtained in canine lower airways. Pharmacologic analysis demonstrated that atropine (10-6 mol/L) blocked the response to both PBTX and acetylcholine; tetrodotoxin (10-7 mol/L) blocked PBTX but not acetylcholine; and verapamil (10-5 mol/L) attenuated but neostigmine (10-8 mol/L) potentiated the response to PBTX. Other selected blockers did not affect the PBTX response. These data indicate that PBTX produces contraction of human lower airway smooth muscle via stimulation of cholinergic nerve fiber sodium channels. The concept that PBTX triggers asthma through this mechanism is strengthened by these results.

Original languageEnglish (US)
Pages (from-to)1187-1191
Number of pages5
JournalJournal of Allergy and Clinical Immunology
Volume81
Issue number6
DOIs
StatePublished - 1988
Externally publishedYes

Fingerprint

Smooth Muscle
Asthma
Sodium Channels
Acetylcholine
Canidae
Harmful Algal Bloom
Cholinergic Fibers
Sneezing
Neostigmine
Vas Deferens
Nerve Endings
Respiratory Sounds
Tetrodotoxin
Verapamil
Atropine
Nerve Fibers
Cough
Adrenergic Agents
Cholinergic Agents
Dogs

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Shimoda, T., Krzanowski, J., Nelson, R., Martin, D. F., Polson, J., Duncan, R., & Lockey, R. (1988). In vitro red tide toxin effects on human bronchial smooth muscle. Journal of Allergy and Clinical Immunology, 81(6), 1187-1191. https://doi.org/10.1016/0091-6749(88)90889-5

In vitro red tide toxin effects on human bronchial smooth muscle. / Shimoda, Terufumi; Krzanowski, Joseph; Nelson, Robert; Martin, Dean F.; Polson, James; Duncan, Robert; Lockey, Richard.

In: Journal of Allergy and Clinical Immunology, Vol. 81, No. 6, 1988, p. 1187-1191.

Research output: Contribution to journalArticle

Shimoda, T, Krzanowski, J, Nelson, R, Martin, DF, Polson, J, Duncan, R & Lockey, R 1988, 'In vitro red tide toxin effects on human bronchial smooth muscle', Journal of Allergy and Clinical Immunology, vol. 81, no. 6, pp. 1187-1191. https://doi.org/10.1016/0091-6749(88)90889-5
Shimoda, Terufumi ; Krzanowski, Joseph ; Nelson, Robert ; Martin, Dean F. ; Polson, James ; Duncan, Robert ; Lockey, Richard. / In vitro red tide toxin effects on human bronchial smooth muscle. In: Journal of Allergy and Clinical Immunology. 1988 ; Vol. 81, No. 6. pp. 1187-1191.
@article{621036749a4540df8745eb0b6ba906f2,
title = "In vitro red tide toxin effects on human bronchial smooth muscle",
abstract = "Airborne Ptychodiscus brevis toxin (PBTX), produced by Ptychodiscus brevis (Florida red tide), induces cough, rhinorrhea, watery eyes, and sneezing in normal individuals and wheezing in subjects with asthma. The mechanism of PBTX-induced contractile response has been investigated by the authors in vitro in dog and rat tissue. PBTX stimulates neuronal sodium channels, resulting in activation of autonomic cholinergic and adrenergic nerve endings in canine upper and lower airway smooth muscle and in rat vas deferens, respectively. This article concerns the investigation of the effect and mechanism of action of PBTX on human airways in order to determine the unique role of the toxin in the pathogenesis of asthma. PBTX elicited contractions of isolated human airway smooth muscle with a threshold concentration of 0.1 μg/ml, a peak response at 12.0 μg/ml, and an effective concentration for 50{\%} of 1.24 μg/ml, very similar to values obtained in canine lower airways. Pharmacologic analysis demonstrated that atropine (10-6 mol/L) blocked the response to both PBTX and acetylcholine; tetrodotoxin (10-7 mol/L) blocked PBTX but not acetylcholine; and verapamil (10-5 mol/L) attenuated but neostigmine (10-8 mol/L) potentiated the response to PBTX. Other selected blockers did not affect the PBTX response. These data indicate that PBTX produces contraction of human lower airway smooth muscle via stimulation of cholinergic nerve fiber sodium channels. The concept that PBTX triggers asthma through this mechanism is strengthened by these results.",
author = "Terufumi Shimoda and Joseph Krzanowski and Robert Nelson and Martin, {Dean F.} and James Polson and Robert Duncan and Richard Lockey",
year = "1988",
doi = "10.1016/0091-6749(88)90889-5",
language = "English (US)",
volume = "81",
pages = "1187--1191",
journal = "Journal of Allergy and Clinical Immunology",
issn = "0091-6749",
publisher = "Mosby Inc.",
number = "6",

}

TY - JOUR

T1 - In vitro red tide toxin effects on human bronchial smooth muscle

AU - Shimoda, Terufumi

AU - Krzanowski, Joseph

AU - Nelson, Robert

AU - Martin, Dean F.

AU - Polson, James

AU - Duncan, Robert

AU - Lockey, Richard

PY - 1988

Y1 - 1988

N2 - Airborne Ptychodiscus brevis toxin (PBTX), produced by Ptychodiscus brevis (Florida red tide), induces cough, rhinorrhea, watery eyes, and sneezing in normal individuals and wheezing in subjects with asthma. The mechanism of PBTX-induced contractile response has been investigated by the authors in vitro in dog and rat tissue. PBTX stimulates neuronal sodium channels, resulting in activation of autonomic cholinergic and adrenergic nerve endings in canine upper and lower airway smooth muscle and in rat vas deferens, respectively. This article concerns the investigation of the effect and mechanism of action of PBTX on human airways in order to determine the unique role of the toxin in the pathogenesis of asthma. PBTX elicited contractions of isolated human airway smooth muscle with a threshold concentration of 0.1 μg/ml, a peak response at 12.0 μg/ml, and an effective concentration for 50% of 1.24 μg/ml, very similar to values obtained in canine lower airways. Pharmacologic analysis demonstrated that atropine (10-6 mol/L) blocked the response to both PBTX and acetylcholine; tetrodotoxin (10-7 mol/L) blocked PBTX but not acetylcholine; and verapamil (10-5 mol/L) attenuated but neostigmine (10-8 mol/L) potentiated the response to PBTX. Other selected blockers did not affect the PBTX response. These data indicate that PBTX produces contraction of human lower airway smooth muscle via stimulation of cholinergic nerve fiber sodium channels. The concept that PBTX triggers asthma through this mechanism is strengthened by these results.

AB - Airborne Ptychodiscus brevis toxin (PBTX), produced by Ptychodiscus brevis (Florida red tide), induces cough, rhinorrhea, watery eyes, and sneezing in normal individuals and wheezing in subjects with asthma. The mechanism of PBTX-induced contractile response has been investigated by the authors in vitro in dog and rat tissue. PBTX stimulates neuronal sodium channels, resulting in activation of autonomic cholinergic and adrenergic nerve endings in canine upper and lower airway smooth muscle and in rat vas deferens, respectively. This article concerns the investigation of the effect and mechanism of action of PBTX on human airways in order to determine the unique role of the toxin in the pathogenesis of asthma. PBTX elicited contractions of isolated human airway smooth muscle with a threshold concentration of 0.1 μg/ml, a peak response at 12.0 μg/ml, and an effective concentration for 50% of 1.24 μg/ml, very similar to values obtained in canine lower airways. Pharmacologic analysis demonstrated that atropine (10-6 mol/L) blocked the response to both PBTX and acetylcholine; tetrodotoxin (10-7 mol/L) blocked PBTX but not acetylcholine; and verapamil (10-5 mol/L) attenuated but neostigmine (10-8 mol/L) potentiated the response to PBTX. Other selected blockers did not affect the PBTX response. These data indicate that PBTX produces contraction of human lower airway smooth muscle via stimulation of cholinergic nerve fiber sodium channels. The concept that PBTX triggers asthma through this mechanism is strengthened by these results.

UR - http://www.scopus.com/inward/record.url?scp=0023916535&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023916535&partnerID=8YFLogxK

U2 - 10.1016/0091-6749(88)90889-5

DO - 10.1016/0091-6749(88)90889-5

M3 - Article

VL - 81

SP - 1187

EP - 1191

JO - Journal of Allergy and Clinical Immunology

JF - Journal of Allergy and Clinical Immunology

SN - 0091-6749

IS - 6

ER -