Immediate Burn Wound Excision Restores Antibody Synthesis to Bacterial Antigen

Early Excision of a Full-Thickness Burn Prevents Peripheral Nerve Conduction Deficits in Mice

“…A study in BALB/c mice demonstrated that early burn wound excision restores the antibody synthesis function of B cells in response to a bacterial antigen stimulus. 52 The BALB/c mice were subjected to a 30 percent burn and excised and grafted at either 6 hours or 72 hours after the burn. B-cell function, which was significantly depressed by the burn injury, was restored to normal with excision at 6 hours but not at 72 hours.…”

Effects of Delayed Wound Excision and Grafting in Severely Burned Children

“…The removal of the burn eschar immediately by early wound excision and grafting potentially breaks the source of wound infection, and reestablishment of the skin barrier by wound coverage potentially improves burninduced diminished immune response to prevent the further bacterial or fungal infection. [19][20][21][22] In this study, we definitively showed that delayed wound excision causes not only significantly more wound bacterial and fungal contamination, but also a higher incidence of invasive wound infection than that seen with early excision within 48 hours. Leaving devitalized tissue on the wound not only allowed increased bacterial and fungal colonization, but also induced increased bacterial and fungal invasion into subcutaneous viable tissue.…”

Contribution of programmed cell death receptor (PD)-1 to Kupffer cell dysfunction in murine polymicrobial sepsis

“…Thus, while enhanced apoptosis is clearly one of the results of this process and the clearance of these apoptotic cells is suggested to have immune-suppressive potential (27,55), it is not the sole cause for the immune dysfunction seen in sepsis. Our laboratory (9,43) and others (31,44,47,61) have shown that the presence of marked tissue injury/damage (in the form of cecal ligation-no puncture, or burn wound) alone is not sufficient to cause marked mortality, yet does appear to play a role in stimulating the differentiation of anti-inflammatory/immune-suppressive macrophage or dendritic cell phenotypes (9,36,37). We have also found that much of the proinflammatory response in cecal ligation and puncture (CLP) mice is mediated through differential activation of various tissue macrophages (7,8), and it appears that the subsequent induction of these divergent immune-suppressive macrophage phenotypes is differentially controlled (16,51).…”