The effects of vitamin A on B cell development in the chick

Vitamin A has been shown to facilitate peripheral B-cell maturation, but its role during B-cell development is unclear. We used a two generation model where hens were fed diets that contained either 2100, 3000 or 3900 IU/kg of vitamin A. Chicks were hatched from eggs that contained 0.88, 1.04, or 1.57 mug retinol/g yolk and fed a diet that contained 1050 IU/kg of VA (VA-), 1500 IU/kg of VA (VAR) or 1950 IU/kg of VA (VA+). At 7, 14, and 21 d of age the bursa was collected. Histological changes of the bursa and the relative mRNA expression for activation induced cytidine deaminase (AID) and Bu-1, a protein marker for developing B cells, were measured. AID expression was significantly depressed in the VA-chicks at 7 d of age, however there was no histological evidence of squamous metaplasia. Bursacytes isolated from VA-chicks had significantly fewer bursal cells, but neither AID nor Bu-1 expression was altered. Next we investigated if the decreased amount of bursacytes was due to an increase in apoptosis and the mechanism that was involved. Both the mean and median intensity of fluorescence of annexin V was brighter in the VA-chicks signifying a higher rate of apoptosis. However, both the caspase 8 and 9 activity was lower in the VA-chicks than the VAR and VA+ chicks. The VA-chicks had significantly lower BAFF expression at 7 d of age from both the VAR and VA+ chicks, while the BAFFR expression from the VA-chicks was only different from the VAR chicks at 7 d of age. In conclusion, VA deficiency results in a decrease in bursacytes, which is caused by an increase in apoptosis.