Inflammatory cell activation in sepsis

被引:53
作者
Bellingan, G [1 ]
机构
[1] Rayne Inst, Bloomsbury Inst Intens Care Med, London WC1E 6JJ, England
关键词
D O I
10.1258/0007142991902277
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The body relies for protection on an effective inflammatory response. To sustain an armoury of inflammatory cells in a state of permanent activation would be impossible and a system whereby such cells can be rapidly activated is, therefore, employed. Upon transition from the resting to activated state inflammatory cells perform multiple defensive functions and are then removed, limiting the duration of inflammation. Neutrophils are the major circulating inflammatory cells but macrophages exert a more powerful regulatory effect. If the inflammatory response is inadequate there is a risk of overwhelming sepsis. By contrast, an unregulated response can lead to systemic inflammation and consequent multiple organ damage. This review focuses on the mechanisms whereby inflammatory cells are activated, how the regulatory system may misfunction and how it may in the future be manipulated to therapeutic advantage.
引用
收藏
页码:12 / 29
页数:18
相关论文
共 49 条
  • [1] Abraham E, 1996, New Horiz, V4, P184
  • [2] ADAMS DO, 1992, INFLAMMATION BASIC P, P673
  • [3] ENDOTHELIAL AND EPITHELIAL-CELL ADHESION MOLECULES
    ALBELDA, SM
    [J]. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1991, 4 (03) : 195 - 203
  • [4] Bellingan GJ, 1996, J IMMUNOL, V157, P2577
  • [5] BELLINGAN GJ, 1999, OXFORD TXB CRITICAL, P898
  • [6] BION JF, 1999, OXFORD TXB CRITICAL, P923
  • [7] DEFINITIONS FOR SEPSIS AND ORGAN FAILURE AND GUIDELINES FOR THE USE OF INNOVATIVE THERAPIES IN SEPSIS
    BONE, RC
    BALK, RA
    CERRA, FB
    DELLINGER, RP
    FEIN, AM
    KNAUS, WA
    SCHEIN, RMH
    SIBBALD, WJ
    [J]. CHEST, 1992, 101 (06) : 1644 - 1655
  • [8] Sir Isaac Newton, sepsis, SIRS, and CARS
    Bone, RC
    [J]. CRITICAL CARE MEDICINE, 1996, 24 (07) : 1125 - 1128
  • [9] Multiple steps in the regulation of transcription-factor level and activity
    Calkhoven, CF
    Ab, G
    [J]. BIOCHEMICAL JOURNAL, 1996, 317 : 329 - 342
  • [10] Neutrophil priming: pathophysiological consequences and underlying mechanisms
    Condliffe, AM
    Kitchen, E
    Chilvers, ER
    [J]. CLINICAL SCIENCE, 1998, 94 (05) : 461 - 471