Effects of Platelet Activating Factor on Various Physiological Parameters of Neutrophils, Alveolar Macrophages, and Alveolar Type II Cells.
Van Dyke-K; Rabovsky-J; Judy-DJ; Pailes-WH; McPeek-M; Sapola-NA; Castranova-V
NIOSH 1990 Nov:1375-1379
The effects of platelet activating factor (PAF) were examined on several physiological parameters of neutrophils, alveolar macrophages, and alveolar type-II epithelial cells. Neutrophils were isolated from human blood by dextran settling and centrifugal elutriation. Rat alveolar macrophages were obtained by pulmonary lavage. Rat alveolar type-II cells were isolated by enzymatic digestion. Measurements were taken of transmembrane potential, respiratory burst activity, and cellular viability. PAF depolarized neutrophils by increasing membrane permeability to sodium. Although PAF depolarized alveolar macrophages, it did not directly activate a respiratory burst. However, PAF treatment did prime the cells to be more responsive to subsequent exposures to particles. Since PAF may be released following dust exposure, the potentiating action of PAF could have important consequences in escalating the cycle of inflammation and tissue damage noted in certain occupational lung diseases. The authors conclude that PAF may be released from phagocytes following occupational exposures. This PAF would be inflammatory by directly activating neutrophils and potentiating the response of macrophages to particulates. In addition, xenobiotic metabolism by alveolar type-II cells would be enhanced affecting the detoxication and/or activation of foreign compounds. The role which these cellular changes play in pneumoconioses remains to be defined.
Lung-irritants; Dust-inhalation; Airborne-dusts; Respiratory-system-disorders; Pulmonary-function; Lung-cells; Alveolar-cells; In-vitro-study;
Asthma and Chronic Obstructive Pulmonary Disease; Disease and Injury; Respiratory-system-disorders;
Proceedings of the VIIth International Pneumoconioses Conference