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Adjuvant-induced arthritic (AA) differentially affects norepinephrine concentrations in immune organs, and  in vivoβ  -adrenergic receptor (  β  -AR) agonist treatment distinctly regulates  ex vivo  cytokine profiles in different immune organs. We examined the contribution of altered   β  -AR functioning in AA to understand these disparate findings. Twenty-one or 28 days after disease induction, we examined   β    2 -AR expression in spleen and draining lymph nodes (DLNs) for the arthritic limbs using radioligand binding and western blots and splenocyte   β  -AR-stimulated cAMP production using enzyme-linked immunoassay (EIA). During severe disease,   β  -AR agonists failed to induce splenocyte cAMP production, and   β  -AR affinity and density declined, indicating receptor desensitization and downregulation. Splenocyte   β    2 -AR phosphorylation (p  β    2 -AR) by protein kinase A (p  β    2 -AR PKA ) decreased in severe disease, and p  β    2 -AR by G protein-coupled receptor kinases (p  β    2 -AR GRK ) increased in chronic disease. Conversely, in DLN cells, p  β    2 -AR PKA  rose during severe disease, but fell during chronic disease, and p  β    2 -AR GRK  increased during both disease stages. A similar p  β    2 -AR pattern in DLN cells with the mycobacterial cell wall component of complete Freund's adjuvant suggests that pattern recognition receptors (i.e., toll-like receptors) are important for DLN p  β    2 -AR patterns. Collectively, our findings indicate lymphoid organ- and disease stage-specific sympathetic dysregulation, possibly explaining immune compartment-specific differences in   β    2 -AR-mediated regulation of cytokine production in AA and rheumatoid arthritis.

Altered Sympathetic-to-Immune Cell Signaling viaβ2-Adrenergic Receptors in Adjuvant Arthritis

Altered Sympathetic-to-Immune Cell Signaling viaβ₂-Adrenergic Receptors in Adjuvant Arthritis