In this regard, since NO is a gas, it is able to diffuse into the abscess thereby reducing bacterial burden and the area of subcutaneous abscesses by inducing vascular permeability and vasodilation. Furthermore, NO stimulates the infiltration of immune cells such as Eupalinolide-A neutrophils, macrophages, and lymphocytes. NO-np can potentially induce a protective immune response capable of containing the infection, therefore preventing systemic dissemination. Another benefit of treatment of MRSA abscesses is the stimulation of healing by induction of collagen deposition. NO promotes wound healing through collagen secretion by fibroblasts. Acceleration of wound healing by nitric oxide donors has been demonstrated previously. Indeed, accelerated healing of gastric ulcers has been demonstrated in rats treated with a nitric oxide-releasing derivative of diclofenac, and a similar effect could be observed by treating the rats with Orientin glyceryl trinitrate. Further, Thornton et al. demonstrated that collagen deposition was enhanced in wounded rats transfected in vivo with the gene for inducible nitric oxide synthase, and the increased nitric production within the wound milieu preceded the observed increase in collagen synthesis. Additionally, we recently suggested that topically applied NO-np might also prevent collagen degradation by bacterial collagenases through a reduction in bacterial burden. Bacteria impair repair processes by producing toxic byproducts and competing with cells for oxygen and nutrients. In treating MRSA subcutaneous abscesses with NO-np, as proposed in our study, we showed that NO-np can modulate immune responses to facilitate the reduction of bacterial burden. This is the highest priority in treating chronic and non-healing abscesses since a persistent infection and accumulation of bacterial antigens, as commonly seen in microbial abscesses, can impair host responses. A persistent infection can further disrupt the normal process of healing by impairing recruitment and migration of immune cells to the site of injury, leading to abnormal levels of cytokines and growth factors.