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SIRS is associated with lymphopenia, and prolonged lymphopenia of septic patients has been associated with increased mortality risk. We hypothesize that elevated adenosine during SIRS down-regulates G-coupled AR, which signals an effect that sensitizes a cAMP-dependent lymphotoxic response. In this study, we evaluate the role of adenosine in SIRS-mediated lymphopenia and impaired IL-15 production. Cecal ligation and puncture was used to induce sepsis-associated SIRS in mice. BMDCs were cultured and used to measure the effect of adenosine on IL-15. We found that AR mRNA levels were significantly down-regulated and AR-dependent G activity was abolished in T cells of septic mice. In accordance, cAMP was elevated in isolated T cells from cecal ligation and puncture compared with sham-treated mice. Similar to septic mice, leukopenia was evident in sham AR-KO mice, after treatment with the AR antagonist (8-cyclopentyl-1,3-dipropylxanthine), or after AR desensitization. In contrast, AR-KO mice were protected from leukopenia. In addition, we observed that septic AR-KO mice exhibited low IL-15 levels. Cultured BMDC agonists of AR and AR inhibited IL-15 production and adenosine blocked IL-15-dependent proliferation of cytotoxic T cells that were cocultured with stimulated BMDCs. To conclude, we suggest that SIRS-associated lymphopenia is initiated by AR desensitization and adenosine-mediated inhibition of IL-15 production is part of the mechanism that accounts for the delay in leukopenia recovery in patients with severe sepsis. Interference with adenosine signaling may thus be potentially beneficial for septic patients with leukopenia.

Background. Adenosine, a potent regulator of inflammation, is produced under stressful conditions due to degradation of ATP/ADP by the ectoenzymes CD39 and CD73. Adenosine is rapidly degraded by adenosine deaminase (ADA) or phosphorylated in the cell by adenosine kinase (AK). From four known receptors to adenosine, A 1 (A 1 R) promotes inflammation by a G i -coupled receptor. We have previously shown that A 1 R is up-regulated in the first hours following bacterial inoculation. The aim of the current study is to characterize the inflammatory mediators that regulate adenosine-metabolizing enzymes and A 1 R at the onset of peritonitis. Methods. Peritonitis was induced in CD1 mice by intraperitoneal injection of Escherichia coli. TNFα and IL-6 levels were determined in peritoneal fluid by enzymelinked immunosorbent assay. Adenosine-metabolizing enzymes and the A 1 R mRNA or protein levels were analyzed by quantitative PCR or by Western blot analysis, respectively. Results. We found that CD39 and CD73 were up-regulated in response to bacterial stimuli (6-fold the basal levels), while AK and ADA mRNA levels were down-regulated. Cytokine production and leukocyte recruitment were enhanced (2.5-fold) by treatment with an A 1 R agonist (2-chloro-N 6 -cyclopentyladenosine, 0.1mg/kg) and reduced (2.5-3-fold) by the A 1 R antagonist (8-cyclopentyl-1, 3-dipropylxanthine, 1mg/kg). In contrast to lipopolysaccharide, IL-1, TNF and IFNγ, only low IL-6 levels (0.01 ng/ml), in the presence of its soluble IL-6R (sIL-6R), were found to promote A 1 R expression on mesothelial cells. In mice, administration of neutralizing antibody to IL-6R or soluble gp130-Fc (sgp130-Fc) blocked peritoneal A 1 R up-regulation following inoculation. Conclusion. Bacterial products induce the production of adenosine by up-regulation of CD39 and CD73. Low IL-6-sIL-6R up-regulates the A 1 R to promote efficient inflammatory response against invading microorganisms.

Adenosine is a potent modulator that has a tremendous effect on the immune system.Adenosine affects T cell activity, and is necessary in maintaining the T helper/regulatory T cell (T reg ) ratio. Adenosine signalling is also involved in activating neutrophils and the formation of neutrophil extracellular traps (NETs), which has been linked to autoimmune disorders. Therefore, adenosine, through its receptors, is extremely important in maintaining homeostasis and involved in the development of autoimmune diseases. In this study, we aim to evaluate the role of adenosine A 1 and A 2A receptors in involvement of autoimmune diseases. We studied adenosine regulation by NETosis in vitro, and used two murine models of autoimmune diseases: type I diabetes mellitus (T1DM) induced by low-dose streptozotocin and pristane-induced systemic lupus erythematosus (SLE). We have found that A 1 R enhances and A 2A R suppresses NETosis. In addition, in both models, A 1 R-knock-out (KO) mice were predisposed to the development of autoimmunity.In the SLE model in wild-type (WT) mice we observed a decline of A 1 R mRNA levels 6 h after pristane injection that was parallel to lymphocyte reduction. Following pristane,