Age-related alterations in IL-1 beta, TNF-alpha, and IL-6 concentrations in parotid acinar cells from BALB/c and non-obese diabetic mice

IL-1 beta, TNF-alpha, and IL-6 have been implicated in the destruction of p arotid gland acinar cells (but not duct cells) in autoimmune sialoadenitis. Here we report the temporal alterations of these cytokines in parotid acin ar cells that may lead to this specificity in cell death in the non-obese d iabetic (NOD) mouse model for Sjogren's syndrome. Immunohistochemistry on p araffin sections of parotid gland from 5- and 10-week-old BALB/c and NOD mi ce confirmed the presence of many peri-acinar lymphoid nodules but few T-ce lls and macrophages between acinar cells. RT-PCR on enzymatically dispersed mouse parotid acinar cells (MPACs) showed no bands for CD3 epsilon, CD20, or F4/80 regardless of mouse strain or age. By ELISA, MPACs from 10-week-ol d NODs showed a small but highly significant (p<0.003) increase in IL-1 bet a and a large significant decrease (p<0.008) in IL-6 compared to 5-week-old NODs. Norepinephrine-stimulated amylase release from MPACs was not differe nt regardless of mouse strain or age. These data show that alterations in a cinar cell production of IL-1 beta and IL-6 in aging NODs precede periducta l lymphoid aggregates and acinar cell secretory dysfunction.