title: Interleukin-1 and the response to injury.
abstract: Traumatic injury is the leading cause of morbidity and mortality in Americans less than 45 years old. People surviving the initial insult undergo metabolic, hemodynamic and immunologic changes which contribute to both early and late complications. Though necessary for normal immunologic response and for wound healing, pathologic alterations of IL-1 synthesis, degradation, and binding to receptors on both a local and systemic level could lead to these changes. Manipulation of IL-1-mediated effects might be of therapeutic utility in the management of trauma in the future.
authors.affiliation: Department of Surgery, New England Medical Center, Boston, Mass.
authors.forename: E
authors.initials: E
authors.lastname: Kaplan
authors.forename: C A
authors.initials: CA
authors.lastname: Dinarello
authors.forename: J A
authors.initials: JA
authors.lastname: Gelfand
mesh_terms: D000818:Animals; D002056:Burns / Q000276:immunology / Q000378:metabolism; D004357:Drug Synergism; D006801:Humans; D007375:Interleukin-1 / Q000276:immunology / Q000502:physiology*; D011817:Rabbits; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000502:physiology; D014945:Wound Healing; D014947:Wounds and Injuries / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology
chemical_list: D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha