title: The effects of chemical sympathectomy on T-cell cytokine responses are not mediated by altered peritoneal exudate cell function or an inflammatory response.
abstract: Ablation of the sympathetic nervous system by chemical sympathectomy is a standard model for the study of sympathetic nervous system regulation of immune function. We have previously documented that chemical denervation results in enhanced antigen-specific, but suppressed mitogen-induced, cytokine production by spleen cells. In our investigation into the mechanisms of sympathectomy-induced immune alterations, we first evaluated the peritoneal environment into which the protein antigen keyhole limpet hemocyanin is administered. Denervation resulted in increased production of tumor necrosis factor-alpha by peritoneal exudate cells and these cells appeared to have enhanced antigen presenting capability. We hypothesized that nerve terminal destruction may be inducing an inflammatory response by monocyte/macrophages and other cell types throughout the periphery that could differentially alter subsequent mitogen versus antigen-specific responses. However, no evidence of sympathectomy-induced systemic or local splenic inflammatory responses was observed, as indicated by measuring the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1beta. These experiments indicate that an inflammatory response is not likely to be responsible for sympathectomy-induced immune alterations, eliminating a potential confounding factor in interpreting sympathectomy studies.
authors.affiliation: Graduate Program in Neuroscience, The Center for Psychoneuroimmunology Research, Rochester, New York 14642, USA.
authors.forename: Tracy A
authors.initials: TA
authors.lastname: Callahan
authors.forename: Jan A
authors.initials: JA
authors.lastname: Moynihan
mesh_terms: D000818:Animals; D002469:Cell Separation; D002999:Clone Cells; D016207:Cytokines / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D005122:Exudates and Transudates / Q000378:metabolism*; D006433:Hemocyanins / Q000276:immunology; D007249:Inflammation / Q000139:chemically induced / Q000473:pathology*; D007371:Interferon-gamma / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D016627:Oxidopamine; D010529:Peritoneal Cavity / Q000166:cytology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013154:Spleen / Q000473:pathology; D013563:Sympathectomy, Chemical; D013565:Sympatholytics; D013601:T-Lymphocytes / Q000378:metabolism*
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D013565:Sympatholytics; D007371:Interferon-gamma; D016627:Oxidopamine; D006433:Hemocyanins; C032808:keyhole-limpet hemocyanin