Inflammation is a self-protecting immune response of the body against harmful stimuli in an attempt to eliminate the stimuli and initiate the healing cascade. Diabetic ulcer is a serious complication associated with type 2 diabetes mellitus. A chronic inflammatory state is a characteristic feature of these ulcers. Resolution of inflammation is a dynamically regulated process the timeliness of which has major bearing on healing outcomes. Macrophages are highly plastic, dynamic and heterogeneous cells that are major regulators of inflammatory response at an injury–site. The diabetic wound healing program funded by NIH NIDDK is investigating role of macrophage plasticity and phenotypes in diabetic ulcers.
Infection is a common complication of chronic ulcers. Biofilms are estimated to account for 60% of chronic wound infections. In biofilm, bacteria are encased within extra polymeric substance (EPS) and become recalcitrant to antimicrobials and host defenses. Using a preclinical swine model of mixed species wound biofilm infection, an unusual observation was made that although biofilm infection may or may not influence the rate of wound closure as measured by standard planimetry, it inevitably compromises the functional property of the repaired skin. The wound may close as evaluated visually, but that closed wound lacks barrier function. Such pathology is caused by the perturbation of epithelial junctional proteins in response to biofilm infection. The wound biofilm infection program funded by multiple awards from NIH NINR is investigating host-biofilm infection interactions and underlying mechanisms of such interactions.