Ozone reduces murine alveolar and peritoneal macrophage phagocytosis: The role of prostanoids

Brendan J Canning, R. R. Hmieleski, Ernst W Spannhake, G. J. Jakab

Research output: Contribution to journalArticle

Abstract

Continuous ozone exposure (0.5 ppm, 1-14 days) reduced the phagocytic activity of murine alveolar and peritoneal macrophages. The response of peritoneal macrophages to ozone was virtually indistinguishable from the response of alveolar macrophages. When added exogenously, prostaglandin E2 (PGE2) inhibited alveolar and peritoneal macrophage phagocytosis. To test the hypothesis that prostanoids mediated the effects of ozone on macrophages, PGE levels of bronchoalveolar lavage fluid (BALF) and the phagocytic activity of macrophages from ozone-exposed mice pretreated with cyclooxygenase inhibitors were measured. PGE levels in BALF were increased following ozone exposure, with high levels of PGE associated with large decreases in phagocytic activity. Pretreatment with indomethacin and d-naproxen completely inhibited ozone-induced increases in PGE recovered by BAL and the suppression of peritoneal macrophage phagocytic activity. The inactive enantiomer of naproxen, I-naproxen, was without effect. Indomethacin partially inhibited ozone-induced suppression of alveolar macrophage phagocytic activity. These observations suggest that prostanoids play a key role in the response to ozone.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume261
Issue number4 5-2
StatePublished - 1991

Fingerprint

Ozone
Alveolar Macrophages
Peritoneal Macrophages
Phagocytosis
Prostaglandins
Prostaglandins E
Naproxen
Bronchoalveolar Lavage Fluid
Indomethacin
Macrophages
Dimercaprol
Cyclooxygenase Inhibitors
Dinoprostone

Keywords

  • cyclooxygenase
  • immunosuppression
  • immunotoxicity
  • indomethacin naproxen
  • oxidants

ASJC Scopus subject areas

  • Cell Biology
  • Physiology
  • Pulmonary and Respiratory Medicine

Cite this

@article{3e496c9012d34262ba01e0b531e07134,
title = "Ozone reduces murine alveolar and peritoneal macrophage phagocytosis: The role of prostanoids",
abstract = "Continuous ozone exposure (0.5 ppm, 1-14 days) reduced the phagocytic activity of murine alveolar and peritoneal macrophages. The response of peritoneal macrophages to ozone was virtually indistinguishable from the response of alveolar macrophages. When added exogenously, prostaglandin E2 (PGE2) inhibited alveolar and peritoneal macrophage phagocytosis. To test the hypothesis that prostanoids mediated the effects of ozone on macrophages, PGE levels of bronchoalveolar lavage fluid (BALF) and the phagocytic activity of macrophages from ozone-exposed mice pretreated with cyclooxygenase inhibitors were measured. PGE levels in BALF were increased following ozone exposure, with high levels of PGE associated with large decreases in phagocytic activity. Pretreatment with indomethacin and d-naproxen completely inhibited ozone-induced increases in PGE recovered by BAL and the suppression of peritoneal macrophage phagocytic activity. The inactive enantiomer of naproxen, I-naproxen, was without effect. Indomethacin partially inhibited ozone-induced suppression of alveolar macrophage phagocytic activity. These observations suggest that prostanoids play a key role in the response to ozone.",
keywords = "cyclooxygenase, immunosuppression, immunotoxicity, indomethacin naproxen, oxidants",
author = "Canning, {Brendan J} and Hmieleski, {R. R.} and Spannhake, {Ernst W} and Jakab, {G. J.}",
year = "1991",
language = "English (US)",
volume = "261",
journal = "American Journal of Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "4 5-2",

}

TY - JOUR

T1 - Ozone reduces murine alveolar and peritoneal macrophage phagocytosis

T2 - The role of prostanoids

AU - Canning, Brendan J

AU - Hmieleski, R. R.

AU - Spannhake, Ernst W

AU - Jakab, G. J.

PY - 1991

Y1 - 1991

N2 - Continuous ozone exposure (0.5 ppm, 1-14 days) reduced the phagocytic activity of murine alveolar and peritoneal macrophages. The response of peritoneal macrophages to ozone was virtually indistinguishable from the response of alveolar macrophages. When added exogenously, prostaglandin E2 (PGE2) inhibited alveolar and peritoneal macrophage phagocytosis. To test the hypothesis that prostanoids mediated the effects of ozone on macrophages, PGE levels of bronchoalveolar lavage fluid (BALF) and the phagocytic activity of macrophages from ozone-exposed mice pretreated with cyclooxygenase inhibitors were measured. PGE levels in BALF were increased following ozone exposure, with high levels of PGE associated with large decreases in phagocytic activity. Pretreatment with indomethacin and d-naproxen completely inhibited ozone-induced increases in PGE recovered by BAL and the suppression of peritoneal macrophage phagocytic activity. The inactive enantiomer of naproxen, I-naproxen, was without effect. Indomethacin partially inhibited ozone-induced suppression of alveolar macrophage phagocytic activity. These observations suggest that prostanoids play a key role in the response to ozone.

AB - Continuous ozone exposure (0.5 ppm, 1-14 days) reduced the phagocytic activity of murine alveolar and peritoneal macrophages. The response of peritoneal macrophages to ozone was virtually indistinguishable from the response of alveolar macrophages. When added exogenously, prostaglandin E2 (PGE2) inhibited alveolar and peritoneal macrophage phagocytosis. To test the hypothesis that prostanoids mediated the effects of ozone on macrophages, PGE levels of bronchoalveolar lavage fluid (BALF) and the phagocytic activity of macrophages from ozone-exposed mice pretreated with cyclooxygenase inhibitors were measured. PGE levels in BALF were increased following ozone exposure, with high levels of PGE associated with large decreases in phagocytic activity. Pretreatment with indomethacin and d-naproxen completely inhibited ozone-induced increases in PGE recovered by BAL and the suppression of peritoneal macrophage phagocytic activity. The inactive enantiomer of naproxen, I-naproxen, was without effect. Indomethacin partially inhibited ozone-induced suppression of alveolar macrophage phagocytic activity. These observations suggest that prostanoids play a key role in the response to ozone.

KW - cyclooxygenase

KW - immunosuppression

KW - immunotoxicity

KW - indomethacin naproxen

KW - oxidants

UR - http://www.scopus.com/inward/record.url?scp=0026014726&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026014726&partnerID=8YFLogxK

M3 - Article

C2 - 1928362

AN - SCOPUS:0026014726

VL - 261

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6135

IS - 4 5-2

ER -