Prolonged Survival of a Skin Homograft in a Patient With Very Extensive Burns

Burn Wound Infections

“…Early observations of the immunodeficiency that follows thermal injury were linked to works on "burn toxins" published by Wertheim, Avdakoff, and Sevitt (17,384,455). More recently, these observations have been supported by the findings of prolonged allograft survival, anergy, and increased susceptibility to infection in burn patients (75,227,324,402,405,462). Despite improvements in the early care of burn patients, systemic inflammatory response syndrome, severe sepsis, and multiple-organ dysfunction syndrome remain major causes of morbidity and mortality (47,194,382).…”

“…Total numbers of T lymphocytes fall in proportion to injury severity during the first week after injury (194,362) and there is a decrease in T-celldependent immune functions (75,227,402,405,462). Diminished T-cell proliferation in response to mitogens (210,364,462) is associated with, and may be the result of, decreased production of IL-2 and IFN-␥ by monocytes (133,463).…”

The Rejection of Skin Homografts in the Normal Human Subject. Part Ii. Histological Findings

“…Scothorne (31) emphasized the changes occurring in the regional lymph nodes after skin grafting, and these have a primary importance in the initial stages of sensitization. In skin grafts placed on burned areas, where the superficial lymphatics are destroyed, the onset of rejection is much delayed (2,32); in one case the graft persisted for 32 weeks (33). Surgical ablation of the regional lymph nodes and lymphatics also prolongs survival (34).…”

The Burn Wound Microenvironment

“…This immunosuppression is evidenced by anergy of the lymphocyte population and consequent prolonged survival of allografts. [21][22][23] Neutrophil dysfunction has also been reported during major burns, 24,25 including reduction of both chemotaxis and degradation of phagocytosed pathogens. 26 Following burn injury, macrophages upregulate expression of PGE 2 and downregulate expression of the proinflammatory cytokine IL-12.…”

“…This in turn leads to decreased lymphocyte proliferation 32,33 with decrease in Tcell-dependent immune functions. [21][22][23] The tilt toward an immunosuppressive response may involve a host of systemic hormone responses from the endocrine system as well as alterations of various signaling cascades, including increases in growth hormone, catecholamines, and cortisol. 17 Increases in glucocorticoids also inhibit proinflammatory cytokine production but not antiinflammatory cytokines.…”