Abstract
Tissue contacting surfaces of medical devices initiate a host inflammatory response, characterized by adsorption of blood proteins and inflammatory cells triggering the release of cytokines, reactive oxygen species (ROS) and reactive nitrogen species (RNS), in an attempt to clear or isolate the foreign object from the body. This normal host response contributes to device-associated pathophysiology and addressing device biocompatibility remains an unmet need. Although widespread attempts have been made to render the device surfaces unreactive, the establishment of a completely bioinert coating has been untenable and demonstrates the need to develop strategies based upon the molecular mechanisms that define the interaction between host cells and synthetic surfaces. In this review, we discuss a family of transmembrane receptors, known as immunoreceptor tyrosine-based inhibitory motif (ITIM)-containing receptors, which show promise as potential targets to address aberrant biocompatibility. These receptors repress the immune response and ensure that the intensity of an immune response is appropriate for the stimuli. Particular emphasis will be placed on the known ITIM-containing receptor, Signal Regulatory Protein Alpha (SIRPhα), and its cognate ligand CD47. In addition, this review will discuss the potential of other ITIM-containing proteins as targets for addressing the aberrant biocompatibility of polymeric biomaterials.
Highlights
The host response to implanted, or extracorporeal, biomaterials is characterized by a nonspecific immune response to the biomaterial [1,2]
The cracking of pacemaker lead insulation, which results in device failure, is mediated by the release of reactive oxygen species (ROS) from monocyte derived macrophages (MDMs) that respond to the polymeric insulation used in pacemaker leads [5,6]
The initiation of the acute inflammatory response starts as a result of the tissue damage that is elicited when the medical device is implanted or, in the case of renal dialysis or cardiopulmonary bypass, when blood is perfused over the synthetic surfaces
Summary
The host response to implanted, or extracorporeal, biomaterials is characterized by a nonspecific immune response to the biomaterial [1,2]. The initiation of the acute inflammatory response starts as a result of the tissue damage that is elicited when the medical device is implanted or, in the case of renal dialysis or cardiopulmonary bypass, when blood is perfused over the synthetic surfaces. This happens immediately after implant or blood material contact and is characterized by the adsorption of blood proteins such as albumin, antibodies, and fibrinogen onto the synthetic surface [8].
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