Aging leads to reduced cellular immunity with consequent increased rates of infectious disease, cancer and autoimmunity in the elderly. The sympathetic nervous system (SNS) modulates innate and adaptive immunity via innervation of lymphoid organs. In aged Fischer 344 (F344) rats, noradrenergic (NA) nerve density in secondary lymphoid organs declines, which may contribute to immunosenescence with aging. These studies suggest there is SNS involvement in age-induced immune dysregulation.
The purpose of this study was to longitudinally characterize age-related change in sympathetic innervation of the spleen and sympathetic activity/tone in male Brown Norway (BN) rats, which live longer and have a strikingly different immune profile than the F344 rat, the traditional animal model for aging research.
Splenic sympathetic neurotransmission was evaluated between 8 and 32 months of age by (1) NA nerve fiber density; (2) splenic norepinephrine (NE) concentration; and (3) circulating catecholamines levels after decapitation.
We report a decline in noradrenergic nerve density in splenic white pulp (45%) at 18 months of age compared with 8 month-old (M) rats, which is followed by a much slower rate of decline between 18 and 32 months. Lower splenic NE concentrations were consistent with morphometric findings. Circulating catecholamines levels generally dropped with increasing age.
These findings suggest there is a sympathetic-to-immune system dysregulation beginning at middle age. Given the unique T-helper-2 bias in Brown Norway rats, altered sympathetic-immune communication may be important for understanding the age-related rise in asthma and autoimmunity.