Book Malte, Chen QiXing, Lehmann Lutz E, Klaschik Sven, Weber Stefan, Schewe Jens-Christian, Luepertz Markus, Hoeft Andreas, Stuber Frank
Department of Anaesthesiology and Intensive Care Medicine, Rheinische-Friedrich-Wilhelms University Bonn, Bonn, Germany.
Crit Care. 2007;11(1):R19. doi: 10.1186/cc5694.
The potent endogenous antimicrobial peptide human beta-defensin 2 (hBD2) is a crucial mediator of innate immunity. In addition to direct antimicrobial properties, different effects on immune cells have been described. In contrast to the well-documented epithelial beta-defensin actions in local infections, little is known about the leukocyte-released hBD2 in systemic infectious disorders. This study investigated the basic expression levels and the ex vivo inducibility of hBD2 mRNA in peripheral whole blood cells from patients with severe sepsis in comparison to non-septic critically ill patients and healthy individuals.
This investigation was a prospective case-control study performed at a surgical intensive care unit at a university hospital. A total of 34 individuals were tested: 16 patients with severe sepsis, 9 critically ill but non-septic patients, and 9 healthy individuals. Serial blood samples were drawn from septic patients, and singular samples were obtained from critically ill non-septic patients and healthy controls. hBD2 mRNA levels in peripheral white blood cells were quantified by real-time polymerase chain reaction in native peripheral blood cells and following ex vivo endotoxin stimulation. Defensin plasma levels were quantified by enzyme-linked immunosorbent assay.
Endotoxin-inducible hBD2 mRNA expression was significantly decreased in patients with severe sepsis compared to healthy controls and non-septic critically ill patients (0.02 versus 0.95 versus 0.52, p < 0.05, arbitrary units). hBD2 plasma levels in septic patients were significantly higher compared to healthy controls and critically ill non-septic patients (541 versus 339 versus 295 pg/ml, p < 0.05).
In contrast to healthy individuals and critically ill non-septic patients, ex vivo inducibility of hBD2 in peripheral blood cells from septic patients is reduced. Impaired hBD2 inducibility may contribute to the complex immunological dysfunction in patients with severe sepsis.
强效内源性抗菌肽人β-防御素2（hBD2）是先天免疫的关键介质。除了直接的抗菌特性外，还描述了其对免疫细胞的不同作用。与局部感染中上皮β-防御素作用的充分记录相比，关于全身感染性疾病中白细胞释放的hBD2知之甚少。本研究调查了严重脓毒症患者外周全血细胞中hBD2 mRNA的基础表达水平和体外诱导性，并与非脓毒症重症患者和健康个体进行比较。
本研究是在一所大学医院的外科重症监护病房进行的一项前瞻性病例对照研究。共测试了34名个体：16名严重脓毒症患者、9名重症但非脓毒症患者和9名健康个体。从脓毒症患者中采集系列血样，从重症非脓毒症患者和健康对照中采集单次血样。通过实时聚合酶链反应对天然外周血细胞和体外内毒素刺激后的外周白细胞中的hBD2 mRNA水平进行定量。通过酶联免疫吸附测定法定量防御素血浆水平。
与健康对照和非脓毒症重症患者相比，严重脓毒症患者内毒素诱导的hBD2 mRNA表达显著降低（0.02对0.95对0.52，p<0.05，任意单位）。脓毒症患者的hBD2血浆水平显著高于健康对照和重症非脓毒症患者（541对339对295 pg/ml，p<0.05）。
与健康个体和重症非脓毒症患者相比，脓毒症患者外周血细胞中hBD2的体外诱导性降低。hBD2诱导性受损可能导致严重脓毒症患者复杂的免疫功能障碍。
