Involvement of the Prokineticin system in animal models of inflammation/neuroinflammation

The immune system constitutes the first line defence against infection or injury and it relies on a large family of Pattern Recognition Receptors (PRRs), which trigger intracellular signalling cascades ultimately culminating in the expression of a variety of proinflammatory molecules, such as cytokines, chemokines, neuropeptides and metabolite of the arachidonic acid cascade. Cytokine and chemokines are involved in peripheral inflammation and neuroinflammation, conditions that differ for the kind of cells and areas involved. Among the mediators responsible of these responses, we can now include the Prokineticin system, a new family of chemokines. In my PhD thesis, I investigated the involvement of Prokineticins in animal models of inflammation and neuroinflammation induced, respectively, by intracolonic infusion of 2,4,6-trinitrobenzene sulfonic acid and intracerebroventricular administration of Amyloid Beta (Aβ1-42) peptide and I have characterized the pharmacological role of PK2β, a peptide derived from proteolytic cleavage of PK2L, a splice variant of pk2 gene.