Wound healing accelerated by Staphylococcus aureus.

While comparing the effects on wound healing of a heated scalpel with those of the cold scalpel, we discovered that inoculation of rat skin incisions with a strain of Staphylococcus aureus dramatically accelerated the gain in wound strength. The accelerating effect was evident four days postoperatively, was maximal at seven to ten days, and was still present at 28 days. The accelerating effect was correlated with the number of S aureus organisms introduced into the wound, and was found in conventional rats and rats germ free up to the time of monocontamination with S aureus. There was no evidence of infection on gross examination; on histologic examination an occasional microabscess was seen in some rats. There may be both local and systemic mechanisms underlying the S aureus accelerating effect. Seven strains of S aureus with varying characteristics demonstrated the wound-healing accelerating effect. In sharp contrast, Staphylococcus epidermidis (three strains), Staphylococcus hominis (one strain), and Pseudomonas aeruginosa (two strains) did not show this effect. The increases in wound healing due to S aureus were substantially greater than reported previously for any nutritional supplement, drug, or other chemical or physical agent.

Accelerating effects of nonviable Staphylococcus aureus, its cell wall, and cell wall peptidoglycan.

We have previously reported that local application of viable Staphylococcus aureus dramatically accelerates wound healing, but viable Staphylococcus epidermidis does not. Because the S. aureus effect occurred in the absence of infection and because the cell walls of the two bacterial species differ, we hypothesized that nonviable S. aureus, its cell wall, and its cell wall component(s) would accelerate healing. Nonviable S. aureus was prepared by chemical and physical means, and its cell wall and peptidoglycan was prepared from heat-killed cultures. In a large number of experiments, nonviable S. aureus (independent of the strain's protein A content), its cell wall, and peptidoglycan when instilled locally at the time of wounding each significantly increased the breaking strength of rat skin incisions (tested both in the fresh state and after formalin fixation). These agents also enhanced subcutaneous polyvinyl alcohol sponge reparative tissue collagen accumulation, generally by a factor of two. Histologic features of treated and control incisions were similar. In contrast, the reparative tissue of treated sponges contained more neutrophils, macrophages, capillaries, and collagen. These experimental data thus confirm our previous studies, as well as our hypothesis, and extend these observations of enhanced wound healing to specific fractions of the bacterial cell wall.