• H Ura, K Hirata, K Yamaguchi, T Katsuramaki, and R Denno.
• First Department of Surgery, Sapporo Medical University School of Medicine, Japan.
• Nihon Geka Gakkai Zasshi. 1998 Aug 1; 99 (8): 485-9.

AbstractMultiple organ failure (MOF) is a critical condition developing in patients with overwhelming bodily injury resulting from major surgical insult, severe trauma, extensive burns, acute pancreatitis, and sepsis. It has recently become evident that the host response to such injury is the main pathogenetic factor contributing to the development of MOF. The proinflammatory cytokines tumor necrosis factor (TNF) and interleukin (IL)-1 are known to play a pivotal role in the pathogenetic mechanisms of MOF. In response to bodily injury, macrophages produce and release TNF and IL-1, which subsequently induce the production of other cytokines (IL-6, IL-8, etc.) and other endogenous chemical mediators. The resultant systemic inflammation may develop into MOF mainly through neutrophil-endothelial cell interaction when the primary injury is overwhelming or a second inflammatory insult such as sepsis triggers an exacerbated inflammation. It has recently been confirmed that the transcription factor NF-kappaB is involved in the up-regulation of a variety of proinflammatory genes and that cell-mediated immunity is down-regulated in the event of major bodily injury through a shift in the balance between T helper 1 (Th1) and Th2 cytokine response patterns. The molecular immunological mechanisms by which these factors participate in the development of MOF should be characterized.

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