THE KINETICS OF CELL PROLIFERATION IN THE TRACHEOBRONCHIAL EPITHELIA OF RATS WITH AND WITHOUT CHRONIC RESPIRATORY DISEASE

Labelling indices of the tracheobronchial epithelia of conventionally-derived rats with chronic respiratory disease (CRD) and minimal-disease rats without CRD have been determined. The duration of the DNA synthesis phase (t_s) computed from the percentage of mitoses labelled at various intervals of time after injection of tritiated thymidine was 7 hr: t_G2 was 3.5 hr. Using the measured value of t_s and the labelling indices, the mean turnover times of the tracheobronchial epithelia in three groups of six 5-week-old conventionally-derived rats were calculated to be 11.2, 14.6 and 22.4 days, while in similar groups of 5-week-old minimal-disease rats the turnover times were found to be 24.3, 36.5 and 41.6 days. The majority of cell divisions in the tracheobronchial epithelium of these minimal disease rats were probably required for growth rather than renewal. The mean turnover time of this tissue in 5-week-old Syrian hamsters was 73 days. The cells of the rat tracheobronchial epithelium have been classed as basal or superficial, depending on their shape and proximity to the basement membrane. The mean turnover time of the basal cells in 5-week-old minimal-disease rats was 11.7 days calculated from labelling indices. The migration method of Brown & Oliver (1968) gave a similar value for the basal cells in minimal-disease rats, and a value of 9.5 days for the basal cells in a group of conventionally-derived rats. The mean turnover time in the latter was only 5.4 days if two rats with tracheobronchitis were included. Consideration of the slow rate of fall in mean grain count over labelled cells at intervals of time after labelling and the calculated turnover times suggests that the proliferative fraction of the basal cell population is close to unity. Well-labelled cells were still present in both basal and superficial populations in the minimal-disease rats at 10 days after labelling. The marked effects of CRD on cell proliferation in this epithelium are emphasized and the significance of this in relation to published work is discussed.