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• W2117620009 abstract "Adjuvant-induced arthritic (AA) differentially affects norepinephrine concentrations in immune organs, and in vivo β -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." @default.
• W2117620009 created "2016-06-24" @default.
• W2117620009 creator A5003395466 @default.
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• W2117620009 date "2013-01-01" @default.
• W2117620009 modified "2023-09-25" @default.
• W2117620009 title "Altered Sympathetic-to-Immune Cell Signaling via<i>β</i>₂-Adrenergic Receptors in Adjuvant Arthritis" @default.
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• W2117620009 doi "https://doi.org/10.1155/2013/764395" @default.
• W2117620009 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3806360" @default.
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