Mucociliary transport in chickens infected with Newcastle disease virus and exposed to sulfur dioxide.

Mucociliary transport was studied in the nasal mucous membranes and sinuses of 3-week-old chickens which were either exposed to sulfur dioxide (SO2), infected intranasally with the mesogenic strain of Newcastle disease virus (NDV), or exposed to SO2 after NDV infection. A newly developed apparatus was used to follow intranasal transport rates over time in the same animal, and to follow sinus transport rates over time in a separate group of animals. Intermittent exposure to concentrations of 1.4-66.0 ppm SO2 produced peaks of increased intranasal transport time, with intervening recovery periods. This suggests a homeostatic mechanism. Transport was also decelerated in the sinus when concentrations of SO2 were above 10 ppm. NDV infection produced decelerated intranasal transport rates but did not decelerate sinus rates. Combined NDV and SO2 interacted to produced persistent deceleration of the intransal transport rate. In the sinus, the combination seemed to conteract the decelerating effect of SO2 alone, suggesting a separate mechanism of homeostasis.