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1.  Chronically lowering sympathetic activity protects sympathetic nerves in spleens from aging F344 rats 
Journal of neuroimmunology  2012;247(1-2):38-51.
In the present study, we investigated how increased sympathetic tone during middle-age affects the splenic sympathetic neurotransmission. Fifteen-month-old F344 rats received rilmenidine (0, 0.5 or 1.5 mg/kg/day, i.p. for 90 days) to lower sympathetic tone. Controls for age were untreated 3 or 18M rats. We report that rilmenidine (1) reduced plasma and splenic norepinephrine concentrations and splenic norepinephrine turnover, and partially reversed the sympathetic nerve loss; and (2) increased β-adrenergic receptor (β-AR) density and β-AR-stimulated cAMP production. Collectively, these findings suggest a protective effect of lowering sympathetic tone on sympathetic nerve integrity, and enhanced sympathetic neurotransmission in secondary immune organs.
doi:10.1016/j.jneuroim.2012.03.022
PMCID: PMC3569974  PMID: 22546498
rilmenidine; imidazoline-1 receptor agonist; sympathetic nervous system; β-adrenergic receptors; cAMP production; aging; splenic norepinephrine turnover
2.  Sympathetic Innervation of the Spleen in Male Brown Norway Rats: A Longitudinal Aging Study 
Brain research  2009;1302:106-117.
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.
Objectives
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.
Methods
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.
Results
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.
Conclusion
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.
doi:10.1016/j.brainres.2009.09.012
PMCID: PMC3622280  PMID: 19748498
noradrenergic nerves; secondary lymphoid organ; stress-induced plasma catecholamines; fluorescence histochemistry; cardiovascular measures; aged
3.  Sympathetic Modulation of Immunity: Relevance to Disease 
Cellular immunology  2008;252(1-2):27-56.
Optimal host defense against pathogens requires cross-talk between the nervous and immune systems. This paper reviews sympathetic-immune interaction, one major communication pathway, and its importance for health and disease. Sympathetic innervation of primary and secondary immune organs is described, as well as evidence for neurotransmission with cells of the immune system as targets. Most research thus far as focused on neural-immune modulation in secondary lymphoid organs, and have revealed complex sympathetic modulation resulting in both potentiation and inhibition of immune functions. SNS-immune interaction may enhance immune readiness during disease- or injury-induced ‘fight’ responses. Research also indicate that dysregulation of the SNS can significantly affect the progression of immune-mediated diseases. However, a better understanding of neural-immune interactions is needed to develop strategies for treatment of immune-mediated diseases that are designed to return homeostasis and restore normal functioning neural-immune networks.
doi:10.1016/j.cellimm.2007.09.005
PMCID: PMC3551630  PMID: 18308299
Noradrenergic; autonomic; sympathetic innervation; lymphoid organs; immune modulation
4.  Fragmentation of Golgi complex and Golgi autoantigens during apoptosis and necrosis 
Arthritis Research  2002;4(4):R3.
Anti-Golgi complex autoantibodies are found primarily in patients with Sjögren's syndrome and systemic lupus erythematosus, although they are not restricted to these diseases. Several Golgi autoantigens have been identified that represent a small family of proteins. Common features of all Golgi autoantigens appear to be their distinct structural organization of multiple α-helical coiled-coil rods in the central domains flanked by non-coiled-coil N-termini and C-termini, and their localization to the cytoplasmic face of Golgi cisternae. Many autoantigens in systemic autoimmune diseases have distinct cleavage products in apoptosis or necrosis and this has raised the possibility that cell death may play a role in the generation of potentially immunostimulatory forms of autoantigens. In the present study, we examined changes in the Golgi complex and associated autoantigens during apoptosis and necrosis. Immunofluorescence analysis showed that the Golgi complex was altered and developed distinctive characteristics during apoptosis and necrosis. In addition, immunoblotting analysis showed the generation of antigenic fragments of each Golgi autoantigen, suggesting that they may play a role in sustaining autoantibody production. Further studies are needed to determine whether the differences observed in the Golgi complex during apoptosis or necrosis may account for the production of anti-Golgi complex autoantibodies.
doi:10.1186/ar422
PMCID: PMC125295  PMID: 12106502
anti-Golgi complex antibody; autoantibody; autoimmunity; cell death

Results 1-4 (4)