Abstract

Neutrophil infiltration to sites of tissue injury occurs during an inflammatory response, and increased numbers of these cells within the pulmonary airspaces have been described in humans and laboratory animals following exposure to ozone (O3), a potent irritant present in photochemical smog. This study examined the effects of O3 on selected secretory and functional activities of human and rabbit neutrophils isolated from peripheral whole blood. Cells were exposed in vitro to 0, 0.1, 0.4, and 1.0 ppm O3 for 2 h. Neutrophil-conditioned medium (NCM) was collected 2 h after exposure and analyzed for the presence of selected eicosanoids. In addition, the phagocytic activity of exposed neutrophils was evaluated by examination of the uptake of latex microspheres. Thromboxane B2 (TxB2) levels were significantly reduced in the NCM from both human and rabbit cells exposed at 1 ppm. The neutrophils from both species showed a significant increase in the production/release of prostaglandin E2 with exposure to 1.0 ppm, while the human cells also exhibited a significant increase at 0.4 ppm. There were no significant O3-related changes in levels of prostaglandin F2α, 6-keto-prostaglandin F1α, or leukotriene B4. Rabbit neutrophils showed a significant increase in phagocytic uptake of latex spheres with exposure to 0.4 and 1.0 ppm O3, whereas the human cells exhibited no change in such activity at any ozone concentration. This study suggests that continued exposure to a pulmonary irritant of neutrophils elicited during an inflammatory response may affect the subsequent activity of these cells. Furthermore, it provides additional data for assessing comparative ozone toxicity in different species.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call