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, USA.
Arch Surg. 1995 Nov;130(11):1186-91; discussion 1191-2. doi: 10.1001/archsurg.1995.01430110044008.
Trauma is believed to activate immunocytes but paradoxically also increases the risk of intraperitoneal infection.
To investigate these events by evaluating changes in the cytokine control networks of human peritoneal macrophages (PM phi) early after trauma.
Case-control study comparing cytokine messenger RNA (mRNA) expression by PM phi from patients with extra-abdominal trauma with that of both peripheral blood mononuclear cells (PBM) and PM phi obtained from healthy individuals.
Level I trauma center and basic science laboratory in a university hospital center.
Six patients with polytrauma (Injury Severity Score, > or = 15) with clinically negative diagnostic peritoneal lavages performed on routine indications at admission to the emergency department and six healthy age- and sex-matched individuals undergoing inguinal herniorrhaphy under local anesthesia.
Peritoneal macrophages were isolated from diagnostic peritoneal lavages in trauma patients. Identical lavages were performed through the hernia sac in the control group.
Cellular RNA was assayed for tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta, IL-6, and IL-10 message by semiquantitative reverse-transcription polymerase chain reaction.
Normal PM phi expressed high levels of TNF-alpha mRNA relative to PBM, but expression of the other proinflammatory cytokines was equivalent to that of PBM. Peritoneal macrophage expression of TNF-alpha mRNA was markedly (64-fold) decreased after trauma (P < .001), when PBM expression of IL-10 mRNA was increased (P = .03).
Human PM phi constitutively show high levels of TNF-alpha message expression, and this is down-regulated by polytrauma. This might constitute a functionally "primed" state. If so, TNF-alpha down-regulation might contribute to functional PM phi suppression after systemic injury.
创伤被认为会激活免疫细胞，但矛盾的是，它也会增加腹腔内感染的风险。
通过评估创伤后早期人类腹腔巨噬细胞（PM phi）细胞因子控制网络的变化来研究这些事件。
病例对照研究，比较腹部外伤患者的PM phi与外周血单核细胞（PBM）以及健康个体的PM phi的细胞因子信使核糖核酸（mRNA）表达。
大学医院中心的一级创伤中心和基础科学实验室。
6例多发伤患者（损伤严重度评分≥15），在急诊科入院时根据常规指征进行了临床诊断性腹腔灌洗结果为阴性，以及6例年龄和性别匹配的健康个体，在局部麻醉下接受腹股沟疝修补术。
从创伤患者的诊断性腹腔灌洗中分离出腹腔巨噬细胞。对照组通过疝囊进行相同的灌洗。
通过半定量逆转录聚合酶链反应检测细胞RNA中的肿瘤坏死因子α（TNF-α）、白细胞介素-1β、IL-6和IL-10信息。
相对于PBM，正常的PM phi表达高水平的TNF-α mRNA，但其他促炎细胞因子的表达与PBM相当。创伤后，PM phi的TNF-α mRNA表达显著降低（64倍）（P<.001），而PBM的IL-10 mRNA表达增加（P=.03）。
人类PM phi持续显示高水平的TNF-α信息表达，并且这会被多发伤下调。这可能构成一种功能上的“预激发”状态。如果是这样，TNF-α下调可能有助于全身损伤后PM phi功能的抑制。
