Abstract
Thermal injury is associated with altered immune defense. Extensive and deep thermal injuries lead to depressed immune defense function with both cellular and humoral defense affected. There is an intricate interaction between various components of the immune system. The altered specific immune response is seen as a depressed ability to produce active rosette-forming cells. Depressed stimulation of lymphocyte proliferation as well as the mixed lymphocyte response have also been recorded following burns. These effects are modulated by the release of kinins, prostaglandins, anaphylatoxins, superoxides, and leukotrienes, all of which can influence the inflammatory response following thermal injury. The humoral immunity is altered as seen by decreased levels of immunoglobulins, activation of complement with release of anaphylatoxins, and formation of membrane attacking complexes leading to inflammation and cytolysis. The immune response to burns is also affected by factors other than this injury, such as nutrition or diseases such as diabetes mellitus or disorders of the lymphoproliferative type. The immune response is also influenced by some drugs used for other reasons such as steroids, chemotherapeutic agents, and topical agents used for burn wound care. The immune reaction to a burn is also influenced by the additive effect of superimposed infections. Removal of injured tissue without the need for extensive transfusion will improve the ability of the burned patients to use their immune defense system in a fruitful way.
Résumé
Les brûlures s'accompagnent d'une altération des mécanismes de défense immunologique. En effet, les brûlures profondes et étendues provoquent une diminution des fonctions cellulaires et humorales, avec des interactions entre les différentes composantes du système immunitaire. Une des traductions de cette dépression de la fonction immunologique est l'incapacité de produire des rosettes. Chez les brûlés, on a décrit également une diminution de la prolifération lymphocytaire et une réponse lymphocytaire mixte. Ces effets sont induits par la libération des kinines, des prostaglandines, des anaphylatoxines, des superoxydes et des leukotriènes, substances qui peuvent influencer la réponse inflammatoire après une agression thermique. L'immunité humorale est altérée comme en attestent la diminution du taux des immunoglobulines, l'activation du complément avec libération des anaphylatoxines et la formation de complexes qui attaquent la membrane cellulaire, entraînant inflammation et cytolyse. La réponse immune aux brûlures est également affectée par d'autres facteurs tel que l'état nutritionnel, certaines pathologies comme le diabète et les maladies lymphoprolifératives. La réponse immune est également influencée par certains médicaments comme les corticoïdes, les antibiotiques et produits à usage local employés dans les soins des brûlures. La réaction immune des brûlures est également perturbée par les surinfections. L'excision des tissus ne s'accompagnant pas de transfusions importantes aidera ces patients à garder leur capital immun.
Resumen
La lesión térmica se asocia con una alteración en la defensa inmunitaria. Las lesiones térmicas extensas y profundas inducen depresión de la función de defensa inmunitaria, afectando tanto los mecanismos de defensa celular como los de defensa humoral. Existe una compleja interacción entre los varios componentes del sistema inmune. La alteración de la respuesta inmunitaria específica se observa como una disimunción de la habilidad para producir células conformadoras de rosetas. Una disminuida estimulación de la proliferación linfocitaria, así como la respuesta linfocítica mixta también han sido registradas en pacientes quemados. Tales efectos son modulados por la liberación de citocinas, prostaglandinas, anafilatoxinas, superóxides y leucotrienos, agentes todos que pueden influenciar la respuesta inflamatoria a la quemadura. La inmunidad humoral resulta alterada a juzgar por niveles disminuidos de inmunoglobulinas, activación del complemento con liberación de anafilatoxinas y formación de complejos que atacan las membranas, lo cual lleva a la inflamación y la citolisis. La respuesta inmunitaria en las quemaduras también resulta afectada por factores diferentes tales como desnutrición, ciertas enfermedades como la diabetes mellitus o entidades de tipo linfoproliferativo. La respuesta inmunitaria también es influenciada por ciertas drogas que se utilizan para otros propósitos, tales como esteroides, algunos agentes quimioterapéuticos y agentes de uso tópico usados para el cuidado de la herida, así como por el efecto aditivo de una infección superpuesta. La remoción de los tejidos lesionados sin la necesidad de grandes transfusiones mejora la capacidad del paciente quemado para utilizar su sistema de defensa inmunitaria en una forma fructífera.
Similar content being viewed by others
References
Ninneman, J.L. Fisher, C.J., Frank, H.A.: Prolonged survival of human skin allografts following thermal injury. Transplantation25:69, 1978
Singh, H., Herndon, D.N., Stein, M.D.: Changes in the population of active rosette-forming cells: A sensitive index for mortality among thermal injury patients. Burns4:85, 1988
Burleson, D.G., Mason, A.D. Jr., Pruitt, B.A. Jr.: Lymphoid subpopulation changes after thermal injury and thermal injury with infection in an experimental model. Ann. Surg.207:208, 1988
Ogle, C.K., Alexander, J.W., Nagy, H., Wood, S., Palkert, D., Carey, M., Ogle, J.D., Warden, G.: A long-term study and correlation of lymphocyte and neutrophil function in the patient with burns. J. Burn Care Rehabil.11:105, 1990
Alexander, J.W., MacMillan, B.G., Stinnett, J.D., Ogle, C., Bozian, R.C., Fisher, J.E., Oakes, J.B., Morris, M.J., Krummel, R.: Beneficial effects of aggressive protein feeding severely burned children. Ann. Surg.192:505, 1980
Bengtsson, A. Heideman, M.: Anaphylatoxin formation in plasma and burn bullae fluid in the thermally injured patient. Burns13:185, 1987
Warden, G.D., Mason, A.D. Jr., Pruitt, B.A. Jr.: Suppression of leukocyte chemotaxis in vitro by chemotherapeutic agents used in the management of thermal injuries. Ann. Surg.181:363, 1975
Graves, T.A., Cioffi, W.G., Mason, A.D. Jr., McManus, W.F., Pruitt, B.A. Jr.: Relationship of transfusion and infection in a burn population. J. Trauma29:948, 1989
Arturson, G., Högman, C.F., Johnsson, S.G.O.: Changes in immunoglobulin levels in severly burned patients. Lancet1:546, 1969
Gelfand, J.A., Donelan, M., Burke, J.F.: Preferential activation and depletion of the alternative complement pathway by burn injury. Ann. Surg.198:58, 1983
Moore, F.D. Jr., Davis, C., Rodrick, M., Mannick, J.A., Fearon, D.T.: Neutrophil activation in thermal injury as assessed by increased expression of complement receptors. N. Engl. J. Med.314:948, 1986
Cavarocchi, N.C., Pluth, J.R., Schaff, H.V., Orszulak, T.A., Homburger, H.A., Solis, E., Kaye, M.P., Clancy, M.S., Kolff, J.: Complement cardiopulmonary bypass: Comparison of bubble and membrane oxygenators. J. Thorac Cardiovasc. Surg.91:252, 1986
Bengtsson, A., Milocco, I., Heideman, M., Berggren, H.: Altered concentrations of terminal complement complexes, anaphylatoxins and leukotrienes in the coronary sinus during cardiopulmonary bypass. J. Cardiothorac. Anesth.3:305, 1989
Ziegler, T.R., Smith, R.J., O'Dwyer, S.T., Demling, R.H., Wilmore, D.W.T.: Increased intestinal permeability associated with infection in burned patients. Arch. Surg.123:1313, 1988
Webster, R.O., Hong, S.R., Johnston, Jr. R.B., Henson, P.M.: Biological effects of the human complement fragments C5a and C5adesArg on neutrophil function. Immunopharmac.2:201, 1980
Bjornson, A.B., Knippenberg, R.W., Bjornson, H.S.: Nonsteroidal anti-inflammatory drugs correct the bactericidal defect of polymorphonuclear leukocytes in a guine pig model of thermal injury. J. Infect. Dis.157:959, 1988
Waymack, J.P., Guzman, R.F., Mason, A.D. Jr., Pruitt, B.A. Jr.: Effect of prostaglandin E in multiple experimental models: Effects on resistance to sepsis. Burns6:9, 1990
Grogan, J.B.: Altered neutrophil phagocytic function in burn patients. J. Trauma16:734, 1976
Fikrig, S.M., Karl, S.C., Suntharalingam, K.: Neutrophil chemotaxis in patients with burns. Ann. Surg.86:746, 1977
Bjornson, A.B., Bjornson, H.S., Altemeier, W.A.: Serum mediated inhibition of polymorphonuclear leukocyte function following burn injury. Ann. Surg.194:224, 1981
Lavaud, P., Mathieu, J., Bienvenu, P., Braquet, M., Gerasimo, P., Kergonou, J.F., Ducousso, R.: Modulation of leukocyte activation in the early phase of the rabbit burn injury. Burns Incl. Therm. Inj.14:15, 1988
Altman, L.C., Furukawa, C.T., Klebanoff, S.J.: Depressed mononuclear leukocyte chemotaxis in thermally injured patients. J. Immunol.119:199, 1977
Schildt, B.E.: Function of RES after thermal and mechanical trauma in mice. Acta Chir. Scand.136:359, 1970
Fletcher, J., Haynes, A.P., Crouch, S.M.: Acquired abnormalities of polymorphonuclear neutrophil function. Blood Rev.4:103, 1990
Koller, M., Konig, W., Brom, J., Erbs, G. Muller, F.E.: Studies on the mechanisms of granulocyte dysfunctions in severely burned patients: Evidence for altered leukotriene generation. J. Trauma29:435, 1989
Dobke, M.K., Hayes, E.C. Baxter, C.R.: Leukotrienes LTB4 and LTC4 in thermally injured patients plasma and burn blister fluid. J. Burn Care Rehabil.8:189, 1987
Marano, M.A., Fong, Y., Moldawer, L.L., Wei, H., Calvano, S.E., Tracey, K.J., Barie, P.S., Manogue, K., Cerami, A., Shires, G.T.: Serum cachectin/tumor necrosis factor in critically ill patients with burns correlates with infection and mortality. Surg. Gynecol. Obstet.170:32, 1990
Howard, R.J.: Effect of burn injury, mechanical trauma, and operation on immune defenses. Surg. Clin. North Am.59:199, 1979
Huang, W.H., Hu, Z.X., Huang, X.Y., Feng, S.Z., Li, A.O.: Abnormalities of serum proteins following thermal injury. Burns15:11, 1989
Alexander, J.W., Wixson, D.: Neutrophil dysfunction and sepsis in burn injury. Surg. Gynecol. Obstet.130:431, 1970
Hugli, T.E.: Structure and function of the anaphylatoxins. Springer Semin. Immunopathol.124:123, 1984
Yurt, R.W., Pruitt, B.A.: Base-line and posthermal injury plasma histamine in rats. J. Appl. Physiol.60:1782, 1986
Bengtsson, A., Heideman, M.: Anaphylatoxin formation in sepsis. Arch. Surg.123:645, 1988
Deitch, E.A., Bridges, R.M., Dobke, M., McDonald, J.C.: Burn wound sepsis may be promoted by a failure of local antibacterial host defenses. Ann. Surg.206:340, 1987
Bengtsson, A., Bengtson, J.P., Rydenhag, Å., Roxvall, L., Heideman, M.: Accumulation of anaphylatoxins and terminal complement complexes in inflammatory fluids. J. Int. Med.228:173, 1990
Gray, D.T., Pine, R.W., Harnar, T.J., Marvin, J.A., Engrav, L.H., Hemback, D.T.: Early surgical excision versus conventional therapy in patients with 20 to 40 per cent burns. Am. J. Surg.144:76, 1982
Sörensen, R., Fisker, N.P., Steensen, J.P.: Acute excision or exposure treatment? Scand. J. Plast. Reconstr. Surg.8:87, 1984
Tompkins, R.G., Burke, J.F., Schoenfeld, D.A., Bondoc, C.C., Quinby, W.C. Jr., Behringer, G.C., Ackroyd, F.W.: Prompt eschar excision: A treatment system contributing reduced burn mortality. Ann. Surg.204:272, 1986
McManus, W.F., Mason, A.D. Jr., Pruitt, B.A. Jr.: Excision of the burn wound in patients with large burns. Arch. Surg.124:718, 1989
Yap, P.L.: Intravenous immunoglobulin for secondary immunodeficiency. Blut60:8, 1990
Kisteler, D., Piert, M., Kauhl, W., Hettich, R.: Use of pseudomonas hyperimmunoglobulin to treat septic shock in burn cases. J. Burn Care Rehabil.10:321, 1977
Saba, T.M., Scovill, W.A.: Effect of surgical trauma on host defense. Surg. Ann.7:71, 1975
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Heideman, M., Bengtsson, A. The immunologic response to thermal injury. World J. Surg. 16, 53–56 (1992). https://doi.org/10.1007/BF02067115
Issue Date:
DOI: https://doi.org/10.1007/BF02067115