The complement factor D (CFD) exerts a regulatory role during infection. However, its physiological function in coagulopathy and its impact on the course of an infection remains unclear. Wild-type and CFD-deficient mice (n = 91) were subjected to cecal ligation and puncture to induce sepsis. At several time points, markers of coagulation and the host-immune response were determined. Furthermore, in patients (n = 79) with sepsis or SIRS, CFD levels were related to clinical characteristics, use of antiplatelet drugs and outcome. Septic CFD-deficient mice displayed higher TAT complexes (p = 0.02), impaired maximal clot firmness, but no relevant platelet drop and reduced GPIIb/IIIa surface expression on platelets (p = 0.03) compared to septic wild-type mice. In humans, higher CFD levels (non-survivors, 5.0 µg/ml to survivors, 3.6 µg/ml; p = 0.015) were associated with organ failure (SOFA score: r = 0.33; p = 0.003) and mortality (75% percentile, 61.1% to 25% percentile, 26.3%). CFD level was lower in patients with antiplatelet drugs (4.5–5.3 µg/ml) than in patients without. In mice, CFD is linked to pronounced platelet activation, depicted by higher GPIIb/IIIa surface expression in wild-type mice. This might be of clinical importance since high CFD plasma concentrations were also associated with increased mortality in sepsis patients.

中文翻译：

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补体因子 D 与人和啮齿动物败血症中的血小板活化有关

补体因子 D (CFD) 在感染过程中发挥调节作用。然而，其在凝血病中的生理功能及其对感染过程的影响仍不清楚。野生型和 CFD 缺陷小鼠 (n = 91) 接受盲肠结扎和穿刺以诱导败血症。在几个时间点，确定了凝血标志物和宿主免疫反应。此外，在脓毒症或 SIRS 患者 (n = 79) 中，CFD 水平与临床特征、抗血小板药物的使用和结果相关。与败血症野生型小鼠相比，败血症 CFD 缺陷小鼠表现出更高的 TAT 复合物（p = 0.02），最大程度的凝块硬度受损，但没有相关的血小板下降和血小板上 GPIIb/IIIa 表面表达降低（p = 0.03）。在人类中，更高的 CFD 水平（非幸存者，5.0 µg/ml 至幸存者，3.6 µg/ml；p = 0。015）与器官衰竭（SOFA 评分：r = 0.33；p = 0.003）和死亡率（75% 百分位，61.1% 至 25% 百分位，26.3%）相关。使用抗血小板药物的患者（4.5-5.3 µg/ml）的 CFD 水平低于未使用的患者。在小鼠中，CFD 与显着的血小板活化有关，在野生型小鼠中表现为更高的 GPIIb/IIIa 表面表达。这可能具有临床重要性，因为高 CFD 血浆浓度也与脓毒症患者死亡率增加有关。