{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T20:50:47Z","timestamp":1774903847669,"version":"3.50.1"},"reference-count":43,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2008,10,30]],"date-time":"2008-10-30T00:00:00Z","timestamp":1225324800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2008,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>The sympathetic nervous system confers a proinflammatory effect during the early phase of type II collagen\u2013induced arthritis (CIA). These effects might be mediated by up\u2010regulation of cytokines such as interferon\u2010\u03b3 (IFN\u03b3) or chemokines such as CXCL1 (cytokine\u2010induced neutrophil chemoattractant, or KC). This study aimed to identify the role of sympathetic neurotransmitters in splenic secretion of IFN\u03b3 and KC shortly after the onset of CIA.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>At different time points during CIA, we determined the density of sympathetic nerve fibers in the spleens of mice. Spleens were removed when the mouse joints were assessed an arthritis score of 3 (at approximately day 32). Spleen slices (0.35 mm thick) were transferred to superfusion microchambers to allow observation of the effects of physiologically released sympathetic neurotransmitters on secretion of IFN\u03b3 and KC.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Compared with control mice, mice with CIA demonstrated a decrease in sympathetic nerve fiber density in the spleens, which reached a minimum density shortly after the start of symptomatic arthritis (day 32). T cell depletion markedly reduced splenic secretion of IFN\u03b3 and KC. Electrical\u2010field stimulation of the spleen slices reduced the secretion of IFN\u03b3, which was attenuated by an \u03b1<jats:sub>1<\/jats:sub>\u2010adrenergic antagonist. In addition, splenic IFN\u03b3 secretion was stimulated by norepinephrine, via \u03b2\u2010adrenergic receptors, and adenosine, via A<jats:sub>1<\/jats:sub> adenosine receptors. Similarly, splenic KC secretion was stimulated by norepinephrine, via \u03b2\u2010adrenergic receptors.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The results of this study demonstrate a reduction of sympathetic nerve fibers in the spleens of arthritic animals. Nevertheless, sympathetic nerves help to increase secretion of IFN\u03b3 and KC, which, at the early stages shortly after the onset of CIA, can contribute to the proinflammatory effect of the sympathetic nervous system.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.24030","type":"journal-article","created":{"date-parts":[[2008,10,30]],"date-time":"2008-10-30T10:59:12Z","timestamp":1225364352000},"page":"3450-3460","source":"Crossref","is-referenced-by-count":62,"title":["Neuronally released sympathetic neurotransmitters stimulate splenic interferon\u2010\u03b3 secretion from T cells in early type II collagen\u2013induced arthritis"],"prefix":"10.1002","volume":"58","author":[{"given":"Rainer H.","family":"Straub","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Luise","family":"Rauch","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexander","family":"Fassold","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Torsten","family":"Lowin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Georg","family":"Pongratz","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2008,10,30]]},"reference":[{"key":"e_1_2_7_2_2","doi-asserted-by":"crossref","first-page":"3423","DOI":"10.1523\/JNEUROSCI.06-12-03423.1986","article-title":"Contribution of sensory afferents and sympathetic efferents to joint injury in experimental arthritis","volume":"6","author":"Levine JD","year":"1986","journal-title":"J Neurosci"},{"key":"e_1_2_7_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0165-5728(94)90006-X"},{"key":"e_1_2_7_4_2","doi-asserted-by":"publisher","DOI":"10.1006\/brbi.1999.0564"},{"key":"e_1_2_7_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.20987"},{"key":"e_1_2_7_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm1551"},{"key":"e_1_2_7_7_2","doi-asserted-by":"publisher","DOI":"10.1186\/ar432"},{"key":"e_1_2_7_8_2","doi-asserted-by":"crossref","first-page":"1958","DOI":"10.4049\/jimmunol.141.6.1958","article-title":"Suppression of murine collagen\u2010induced arthritis with monoclonal anti\u2010Ia antibodies and augmentation with IFN\u2010\u03b3","volume":"141","author":"Cooper SM","year":"1988","journal-title":"J Immunol"},{"key":"e_1_2_7_9_2","doi-asserted-by":"crossref","first-page":"1500","DOI":"10.4049\/jimmunol.142.5.1500","article-title":"Heterogeneous effects of IFN\u2010\u03b3 in adjuvant arthritis","volume":"142","author":"Jacob CO","year":"1989","journal-title":"J Immunol"},{"key":"e_1_2_7_10_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.1990.tb05353.x"},{"key":"e_1_2_7_11_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830250508"},{"key":"e_1_2_7_12_2","doi-asserted-by":"crossref","first-page":"5501","DOI":"10.4049\/jimmunol.158.11.5501","article-title":"High susceptibility to collagen\u2010induced arthritis in mice lacking IFN\u2010\u03b3 receptors","volume":"158","author":"Manoury\u2010Schwartz B","year":"1997","journal-title":"J Immunol"},{"key":"e_1_2_7_13_2","doi-asserted-by":"crossref","first-page":"5507","DOI":"10.4049\/jimmunol.158.11.5507","article-title":"Accelerated collagen\u2010induced arthritis in IFN\u2010\u03b3 receptor\u2010deficient mice","volume":"158","author":"Vermeire K","year":"1997","journal-title":"J Immunol"},{"key":"e_1_2_7_14_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.10832"},{"key":"e_1_2_7_15_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.179.4.2300"},{"key":"e_1_2_7_16_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.179.9.6228"},{"key":"e_1_2_7_17_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.1997.68041633.x"},{"key":"e_1_2_7_18_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.274.4.R997"},{"key":"e_1_2_7_19_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-5728(02)00035-8"},{"key":"e_1_2_7_20_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.166.1.232"},{"key":"e_1_2_7_21_2","doi-asserted-by":"crossref","first-page":"3766","DOI":"10.4049\/jimmunol.140.11.3766","article-title":"Effects of in vivo administration of anti\u2010T3 monoclonal antibody on T cell function in mice. 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