The role of platelet-activating factor in the pulmonary response to inhaled bacterial endotoxin

R. C. Lantz, G. E. Keller, R. Burrell

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Quantitative morphometric analyses were carried out on animals subjected to aerosols of bacterial endotoxin (LPS) to further define the role of platelet-activating factor (PAF) in the development of pulmonary injury. Hamsters were exposed to either saline aerosol or dilute aerosols of LPS (4 μg/m3) for standard lengths of time. Within each aerosol exposure group, animals were further subdivided into groups receiving either the PAF receptor binding antagonist, RP 48740, or saline injections. LPS inhalation resulted in decreased fixed lung volume, increased sequestration of polymorphonuclear leukocytes and platelets in pulmonary capillaries, increased type I epithelial and endothelial cellular volumes, increased cellular interstitium, and increased endothelial pinocytotic vesicles. Treatment with RP 48740 either attenuated or abolished the ability of inhaled LPS to induce these structural alterations. The PAF antagonist also inhibited LPS-induced increases in pulmonary capillary permeability. It is concluded that PAF is one of the major injury-promoting mediators released upon inhalation exposure to environmentally realistic concentrations of bacterial endotoxin. A major but not exclusive target of this mediator is the pulmonary vascular endothelium.

Original languageEnglish (US)
Pages (from-to)167-172
Number of pages6
JournalAmerican Review of Respiratory Disease
Volume144
Issue number1
DOIs
StatePublished - Jan 1 1991

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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