A study in Journal of Neuroimmunology suggests that aging is linked to significant alterations in the sympathetic nervous innervation of lymphoid organs that may contribute to aging-related immunosuppression,
The sympathetic nervous system (SNS) is a major branch of the autonomic nervous system and the peripheral stress system. The function of the human SNS is altered by aging, and these changes involve both the properties of the adrenergic receptors and the outﬂow of sympathetic neural trafﬁc to individual organs.
Recent evidence indicates that progressive sympathetic (noradrenergic) activation occurs with aging. This involves sympathetic outﬂow to the heart, skeletal muscle vasculature, the gut and liver, but excludes the kidneys, and is accompanied by reduced adrenal medullary secretion of epinephrine (M Esler et al., Am J Physiol Regulatory Integrative Comp Physiol 282:R909, 2002).
Previous studies also indicate that sympathetic (noradrenergic) nerve ﬁbers in primary and secondary lymphoid organs undergo age associated alterations in their density, distribution in the parenchyma, norepinephrine (NE) concentrations, NE uptake and release, and beta-adrenergic receptor-induced signaling in rodents. Specifically, thymic involution is associated with increased noradrenergic nerve ﬁber density and NE concentration, while there is a decline in noradrenergic neuronal density and NE concentrations in spleen and lymph nodes in male rats and mice.
In the Journal of Neuroimmunology study Srinivasan ThyagaRajan and colleagues from Loma Linda University School of Medicine, Loma Linda, California, report that the density of sympathetic (noradrenergic) nerve ﬁbers increased signiﬁcantly in all the compartments of thymuses but especially in the cortex and paracortex, associated with a reduced tissue volume and an increase in NE concentration in aged female Fischer 344 rats.
However, sympathetic innervation and NE levels declined in spleen and mesenteric lymph nodes, and was accompanied by signiﬁcant reductions in NK cell activity, IL-2 and IFN-gamma production, and T and B cell proliferation in older female rats.
The rapid decline in sympathetic innervation of secondary lymphoid organs in female rats is consistent with the loss of sympathetic (noradrenergic) innervation previously reported in male rats that had grown older. According to the authors this may indicate the presence of age-related sympathetic peripheral neuropathy, associated with an increase in the NE turnover and impairment in beta-adrenergic receptor signal transduction in these lymphoid organs.
These observations in rodents, and the human data mentioned above suggest that alterations in sympathetic (noradrenergic) innervation, SNS activity and outﬂow, and the sympathetic-immune interface may be causally involved and implicated in a variety of cardiovascular disorders, certain types of autoimmune diseases, cancer, infections, and Alzheimer’s disease, for all of which incidence rises with age.
SOURCE: J Neuroimmunol 2011, 233:54. Epub 2010 Dec 24.