Relationship of interleukin-10 plasma levels to severity of injury and clinical outcome in injured patients

被引:187
作者
Neidhardt, R [1 ]
Keel, M [1 ]
Steckholzer, U [1 ]
Safret, A [1 ]
Ungethuem, U [1 ]
Trentz, O [1 ]
Ertel, W [1 ]
机构
[1] UNIV ZURICH,DIV TRAUMA SURG,CH-8006 ZURICH,SWITZERLAND
关键词
trauma; multiple injury; interleukin-10; sepsis; ARDS; MODS;
D O I
10.1097/00005373-199705000-00017
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Interleukin-10 (IL-10) markedly inhibits lymphocyte and phagocytic functions, which are essential for an adequate immune response to invading microbes. Although various animal and clinical studies revealed an increased release of IL-10 during sepsis, alterations of circulating IL-10 after injury and potential relationships to severity of injury and clinical outcome are unknown, Injured patients (n = 417) showed elevated (p < 0.001) IL-10 levels throughout the observation period of 21 days compared with healthy volunteers (n = 137), Patients with severe injury (Injury Severity Score greater than or equal to 25 points) demonstrated significantly increased IL-10 levels compared with patients with minor trauma (Injury Severity Score < 25 points), Patients who died from injury or developed posttraumatic complications (sepsis, multiple organ dysfunction syndrome) revealed elevated IL-IO levels in comparison with injured patients with uneventful posttraumatic course, Thus, trauma causes an enhanced release of IL-10 dependent on the severity of injury, Because increased IL-10 levels are significantly related to posttraumatic complications, IL-IO may be involved in their pathogenesis.
引用
收藏
页码:863 / 870
页数:8
相关论文
共 45 条
[1]  
American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference, 1992, CRIT CARE MED, V6, P864
[2]   MACROPHAGE DEACTIVATION BY INTERLEUKIN-10 [J].
BOGDAN, C ;
VODOVOTZ, Y ;
NATHAN, C .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 174 (06) :1549-1555
[3]   THE PATHOGENESIS OF SEPSIS [J].
BONE, RC .
ANNALS OF INTERNAL MEDICINE, 1991, 115 (06) :457-469
[4]   INTERLEUKIN-10 (IL-10) INHIBITS THE RELEASE OF PROINFLAMMATORY CYTOKINES FROM HUMAN POLYMORPHONUCLEAR LEUKOCYTES - EVIDENCE FOR AN AUTOCRINE ROLE OF TUMOR-NECROSIS-FACTOR AND IL-1-BETA IN MEDIATING THE PRODUCTION OF IL-8 TRIGGERED BY LIPOPOLYSACCHARIDE [J].
CASSATELLA, MA ;
MEDA, L ;
BONORA, S ;
CESKA, M ;
CONSTANTIN, G .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 178 (06) :2207-2211
[5]   INDUCTION OF INTERFERON-GAMMA PRODUCTION BY NATURAL-KILLER-CELL STIMULATORY FACTOR - CHARACTERIZATION OF THE RESPONDER CELLS AND SYNERGY WITH OTHER INDUCERS [J].
CHAN, SH ;
PERUSSIA, B ;
GUPTA, JW ;
KOBAYASHI, M ;
POSPISIL, M ;
YOUNG, HW ;
WOLF, SF ;
YOUNG, D ;
CLARK, SC ;
TRINCHIERI, G .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 173 (04) :869-879
[6]  
CUNNA FQ, 1992, BIOCHEM BIOPH RES CO, V182, P1155
[7]   INTERLEUKIN-10 (IL-10) INHIBITS HUMAN LYMPHOCYTE INTERFERON GAMMA-PRODUCTION BY SUPPRESSING NATURAL-KILLER-CELL STIMULATORY FACTOR/IL-12 SYNTHESIS IN ACCESSORY CELLS [J].
DANDREA, A ;
ASTEAMEZAGA, M ;
VALIANTE, NM ;
MA, XJ ;
KUBIN, M ;
TRINCHIERI, G .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 178 (03) :1041-1048
[8]   CHARACTERIZATION OF MONOCLONAL-ANTIBODIES AGAINST HUMAN INTERLEUKIN-10 AND THEIR USE IN AN ELISA FOR THE MEASUREMENT OF THIS CYTOKINE [J].
DEGROOTE, D ;
MARCHANT, A ;
FAUCHET, F ;
JADOUL, M ;
DEHART, I ;
GERARD, C ;
GEVAERT, Y ;
LOPEZ, M ;
GATHY, R ;
FRANSSEN, JD ;
RADOUX, D ;
FRANCHIMONT, P .
JOURNAL OF IMMUNOLOGICAL METHODS, 1994, 177 (1-2) :225-234
[9]   HIGH-LEVELS OF INTERLEUKIN-10 DURING THE INITIAL PHASE OF FULMINANT MENINGOCOCCAL SEPTIC SHOCK [J].
DERKX, B ;
MARCHANT, A ;
GOLDMAN, M ;
BIJLMER, R ;
VANDEVENTER, S .
JOURNAL OF INFECTIOUS DISEASES, 1995, 171 (01) :229-232
[10]  
Ertel W, 1996, ARCH SURG-CHICAGO, V131, P51