Hauser C J, Lagoo S, Lagoo A, Hale E, Hardy K J, Barber W H, Bass J D, Poole G V
Department of Surgery, University of Mississippi Medical Center, Jackson 39216-4505, USA.
Shock. 1995 Oct;4(4):247-50. doi: 10.1097/00024382-199510000-00003.
Injury has been hypothesized to cause inflammation through systemic release of lipopolysaccharide and pro-inflammatory cytokines, but this has proved difficult to demonstrate in humans. We looked for evidence of an inflammatory pattern of cytokine gene expression by peripheral blood mononuclear cells (PBM) in six polytraumatized patients (ISS = 25 +/- 8) upon ER admission, and in six matched healthy controls. PBM tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-4, IL-6, IL-10, and interferon (IFN)-gamma message was assessed by semi-quantitative reverse-transcription polymerase chain reaction. No increase in expression of any of the pro-inflammatory cytokines (tumor necrosis factor-alpha, IL-1 beta, or IL-6) was found after trauma, and IFN-gamma tended to decrease. Of the immunosuppressive cytokines, IL-10 expression increased 5-fold (p < .05) but no change in IL-4 was discerned. This pattern is fundamentally different from the cytokine expression patterns expected with sepsis or exposure to lipopolysaccharide. These findings are inconsistent with the occurrence of systemic endotoxemia and subsequent global immunocyte activation early after trauma.
有假说认为，损伤通过脂多糖和促炎细胞因子的全身释放引发炎症，但这一点在人类中很难得到证实。我们在6名多发伤患者（损伤严重度评分=25±8）入院时及6名匹配的健康对照者中，寻找外周血单个核细胞（PBM）细胞因子基因表达炎症模式的证据。通过半定量逆转录聚合酶链反应评估PBM肿瘤坏死因子（TNF）-α、白细胞介素（IL）-1β、IL-4、IL-6、IL-10和干扰素（IFN）-γ的信息。创伤后未发现任何促炎细胞因子（肿瘤坏死因子-α、IL-1β或IL-6）表达增加，且IFN-γ有下降趋势。在免疫抑制细胞因子中，IL-10表达增加了5倍（p<0.05），但未发现IL-4有变化。这种模式与脓毒症或接触脂多糖时预期的细胞因子表达模式根本不同。这些发现与创伤后早期发生全身内毒素血症及随后的整体免疫细胞激活不一致。
