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Irritable bowel syndrome (IBS) is a disease in which, typically, alterations in intestinal motility and visceral hypersensitivity appear to exist, apparently without any organic alteration (Thompson, 1991). Several pathogenic factors responsible for IBS have been suggested. It seems that there are cell factors, which give reason to believe that there is a low-grade intestinal inflammation in this pathology (Ortiz-Lucas et al., 2010). Several cytokines, such as tumour necrosis factor α (TNFα), interleukin 1, and interleukin 6, contribute to the pathogenesis (Ardizzone and Bianchi Porro, 2005; Pizarro et al., 2006). Macrophages are the major producers of TNFα, and, interestingly, they are also highly responsive to TNFα. TNFα has been shown to play a pivotal role in activating the cytokine cascade in many inflammatory diseases and it has been proposed as a therapeutic target for a number of diseases. Consequently, recent strategies for the treatment of intestinal inflammation have primarily targeted the immunopathogenic processes that mediate intestinal inflammation at the cytokine level (Bamias et al., 2003; Sandborm and Targan, 2002). At present, pharmacotherapy represents the mainstay of inflammatory bowel disease management (Stein and Hanauer, 1999). Some anti-inflammatory or immuno-modulating drugs, including salicylates and methotrexate, are able to decrease intracellular adenosine 5 -triphosphate concentrations and raise extracellular adenosine levels. It has been proposed that such properties can significantly contribute to the drugs’ pharmacological actions in inflammatory diseases (Cronstein et al., 1999). Several lines of evidence suggest that adenosine regulates immunity and inflammation (Amann and Peskar, 2002; Montesinos et al., 2007). The wide distribution of adenosine receptors (AR) as well as enzymes for purine metabolism in different gut regions suggests a complex role for this mediator in the regulation of gastrointestinal functions (Antonioli et al., 2008). Adenosine binds to four different types of G protein-coupled cell surface receptors referred to as A1R, A2AR, A2BR, and A3R, each having a unique pharmacological profile, tissue distribution and signalling pathway (Jacobson and Gao, 2006). All known ARs

Adenosine Receptors: New Targets to Protect Against Tissue Damage in Inflammatory Bowel Symptoms