Effect of eotaxin and platelet-activating factor on airway inflammation and hyperresponsiveness in guinea pigs in vivo

Satoru Fukuyama, Hiromasa Inoue, Hisamichi Aizawa, Masahiro Oike, Motoji Kitaura, Osamu Yoshie, Nobuyuki Hara

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Although eotaxin causes selective infiltration of eosinophils into the lung, its role in airway hyperresponsiveness remains unclear. We studied the effects of local administration of eotaxin on airway inflammation and hyperresponsiveness in guinea pigs in vivo. Airway responsiveness to inhaled histamine and differential cell counts in bronchoalveolar lavage fluid (BALF) were evaluated 12 h, 24 h, 3 d, and 7 d after intratracheal instillation of eotaxin. Significant eosinophilia in BALF was observed between 6 h and 7 d after eotaxin administration. Histologically, eosinophil accumulation was observed in the airways but not in the alveoli. In contrast, eotaxin did not affect airway responsiveness between 12 h and 7 d after its administration. We then studied the effects on airway responsiveness of subthreshold doses of interleukin 5, leukotriene D4 (LTD4), and platelet-activating factor (PAF) combined with eotaxin. Neither interleukin 5 nor LTD4 affected airway responsiveness. After eotaxin treatment, PAF significantly enhanced airway responsiveness without further increases in eosinophil counts. Eotaxin plus PAF significantly increased in eosinophil peroxidase activity in BALF compared with control and with eotaxin alone. These data indicate that eotaxin alone causes eosinophil accumulation in the airways but not hyperresponsiveness, and that additional factors such as PAF are needed to activate eosinophils for the development of airway hyperresponsiveness.

Original languageEnglish
Pages (from-to)1844-1849
Number of pages6
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume161
Issue number6
DOIs
Publication statusPublished - Jan 1 2000
Externally publishedYes

Fingerprint

Platelet Activating Factor
Eosinophils
Guinea Pigs
Inflammation
Bronchoalveolar Lavage Fluid
Leukotriene D4
Interleukin-5
Eosinophil Peroxidase
Eosinophilia
Histamine
Cell Count
Lung

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine

Cite this

Effect of eotaxin and platelet-activating factor on airway inflammation and hyperresponsiveness in guinea pigs in vivo. / Fukuyama, Satoru; Inoue, Hiromasa; Aizawa, Hisamichi; Oike, Masahiro; Kitaura, Motoji; Yoshie, Osamu; Hara, Nobuyuki.

In: American Journal of Respiratory and Critical Care Medicine, Vol. 161, No. 6, 01.01.2000, p. 1844-1849.

Research output: Contribution to journalArticle

@article{8404b38e8f4f48ddab2fcaf9af910a9d,
title = "Effect of eotaxin and platelet-activating factor on airway inflammation and hyperresponsiveness in guinea pigs in vivo",
abstract = "Although eotaxin causes selective infiltration of eosinophils into the lung, its role in airway hyperresponsiveness remains unclear. We studied the effects of local administration of eotaxin on airway inflammation and hyperresponsiveness in guinea pigs in vivo. Airway responsiveness to inhaled histamine and differential cell counts in bronchoalveolar lavage fluid (BALF) were evaluated 12 h, 24 h, 3 d, and 7 d after intratracheal instillation of eotaxin. Significant eosinophilia in BALF was observed between 6 h and 7 d after eotaxin administration. Histologically, eosinophil accumulation was observed in the airways but not in the alveoli. In contrast, eotaxin did not affect airway responsiveness between 12 h and 7 d after its administration. We then studied the effects on airway responsiveness of subthreshold doses of interleukin 5, leukotriene D4 (LTD4), and platelet-activating factor (PAF) combined with eotaxin. Neither interleukin 5 nor LTD4 affected airway responsiveness. After eotaxin treatment, PAF significantly enhanced airway responsiveness without further increases in eosinophil counts. Eotaxin plus PAF significantly increased in eosinophil peroxidase activity in BALF compared with control and with eotaxin alone. These data indicate that eotaxin alone causes eosinophil accumulation in the airways but not hyperresponsiveness, and that additional factors such as PAF are needed to activate eosinophils for the development of airway hyperresponsiveness.",
author = "Satoru Fukuyama and Hiromasa Inoue and Hisamichi Aizawa and Masahiro Oike and Motoji Kitaura and Osamu Yoshie and Nobuyuki Hara",
year = "2000",
month = "1",
day = "1",
doi = "10.1164/ajrccm.161.6.9905039",
language = "English",
volume = "161",
pages = "1844--1849",
journal = "American Journal of Respiratory and Critical Care Medicine",
issn = "1073-449X",
publisher = "American Thoracic Society",
number = "6",

}

TY - JOUR

T1 - Effect of eotaxin and platelet-activating factor on airway inflammation and hyperresponsiveness in guinea pigs in vivo

AU - Fukuyama, Satoru

AU - Inoue, Hiromasa

AU - Aizawa, Hisamichi

AU - Oike, Masahiro

AU - Kitaura, Motoji

AU - Yoshie, Osamu

AU - Hara, Nobuyuki

PY - 2000/1/1

Y1 - 2000/1/1

N2 - Although eotaxin causes selective infiltration of eosinophils into the lung, its role in airway hyperresponsiveness remains unclear. We studied the effects of local administration of eotaxin on airway inflammation and hyperresponsiveness in guinea pigs in vivo. Airway responsiveness to inhaled histamine and differential cell counts in bronchoalveolar lavage fluid (BALF) were evaluated 12 h, 24 h, 3 d, and 7 d after intratracheal instillation of eotaxin. Significant eosinophilia in BALF was observed between 6 h and 7 d after eotaxin administration. Histologically, eosinophil accumulation was observed in the airways but not in the alveoli. In contrast, eotaxin did not affect airway responsiveness between 12 h and 7 d after its administration. We then studied the effects on airway responsiveness of subthreshold doses of interleukin 5, leukotriene D4 (LTD4), and platelet-activating factor (PAF) combined with eotaxin. Neither interleukin 5 nor LTD4 affected airway responsiveness. After eotaxin treatment, PAF significantly enhanced airway responsiveness without further increases in eosinophil counts. Eotaxin plus PAF significantly increased in eosinophil peroxidase activity in BALF compared with control and with eotaxin alone. These data indicate that eotaxin alone causes eosinophil accumulation in the airways but not hyperresponsiveness, and that additional factors such as PAF are needed to activate eosinophils for the development of airway hyperresponsiveness.

AB - Although eotaxin causes selective infiltration of eosinophils into the lung, its role in airway hyperresponsiveness remains unclear. We studied the effects of local administration of eotaxin on airway inflammation and hyperresponsiveness in guinea pigs in vivo. Airway responsiveness to inhaled histamine and differential cell counts in bronchoalveolar lavage fluid (BALF) were evaluated 12 h, 24 h, 3 d, and 7 d after intratracheal instillation of eotaxin. Significant eosinophilia in BALF was observed between 6 h and 7 d after eotaxin administration. Histologically, eosinophil accumulation was observed in the airways but not in the alveoli. In contrast, eotaxin did not affect airway responsiveness between 12 h and 7 d after its administration. We then studied the effects on airway responsiveness of subthreshold doses of interleukin 5, leukotriene D4 (LTD4), and platelet-activating factor (PAF) combined with eotaxin. Neither interleukin 5 nor LTD4 affected airway responsiveness. After eotaxin treatment, PAF significantly enhanced airway responsiveness without further increases in eosinophil counts. Eotaxin plus PAF significantly increased in eosinophil peroxidase activity in BALF compared with control and with eotaxin alone. These data indicate that eotaxin alone causes eosinophil accumulation in the airways but not hyperresponsiveness, and that additional factors such as PAF are needed to activate eosinophils for the development of airway hyperresponsiveness.

UR - http://www.scopus.com/inward/record.url?scp=0034048053&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034048053&partnerID=8YFLogxK

U2 - 10.1164/ajrccm.161.6.9905039

DO - 10.1164/ajrccm.161.6.9905039

M3 - Article

C2 - 10852755

AN - SCOPUS:0034048053

VL - 161

SP - 1844

EP - 1849

JO - American Journal of Respiratory and Critical Care Medicine

JF - American Journal of Respiratory and Critical Care Medicine

SN - 1073-449X

IS - 6

ER -