Role of DAMPS-CD14-MYD88 in modulation of inflammatory immune response and tissue repair after implantation 'classic' BIMATERIALS (titanium and ePTFE) in mice

Abstract

Studies have shown that the nature (transient or chronic) and the magnitude of the inflammatory and immunological response, generated by a biomaterial, may be decisive in the implant success or failure. However, it not yet knows how this response is generated, if by direct contact with the biomaterial or by molecules originated by tissue damage resulting from the implantation, such as DAMPs (damage-associated molecular patterns). In general, DAMPs interact with the receptors present in different cell populations collectively termed pattern recognition receptors (PRRs), resulting in induction of inflammatory responses, which may vary in nature and intensity depending on several factors, as the type of initial stimulus, activation pathway triggered, signal intensity and duration. Thus, our hypothesis is that cellular activation via DAMPs-CD14 and DAMPs-MyD88 is responsible for developing a transient inflammatory response of low magnitude, which in turn contributes to the subsequent process of repair after implantation of the biomaterial. The aim of this study is evaluate the role of DAMPs-CD14/MyD88 in the development of inflammatory and immune response and the mechanisms involved in the recognition and repair foward to implantation of 'classic' biomaterials (titanium disks and non-resorbable ePTFE membrane) in mice, according to histomorphometric analysis, enzymatic and molecular levels.