An exacerbated amount of neutrophil extracellular traps (NETs) can cause dysfunction of systems during inflammation. However, host proteins and factors that suppress NET formation (NETosis) are not clearly identified. Here we show that an innate immune collectin, pulmonary surfactant protein-D (SP-D), attenuates lipopolysaccharide (LPS)-mediated NETosis in human neutrophils by binding to LPS. SP-D deficiency in mice (Sftpd -/-) leads to excess NET formation in the lungs during LPS-mediated inflammation. In the absence of SP-D, NETs inhibit the surface-active properties of lung surfactant, essential to prevent the collapse of alveoli, the air breathing structures of the lungs. SP-D reverses NET-mediated inhibition of surfactant and restores the biophysical properties of surfactant. To the best of our knowledge, this study establishes for the first time that (i) SP-D suppresses LPS-mediated NETosis, (ii) NETs inhibit pulmonary surfactant function in the absence of SP-D, and (iii) SP-D can restore NET-mediated inhibition of the surfactant system.

中文翻译：

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SP-D 减弱 LPS 诱导的人中性粒细胞胞外陷阱 (NET) 的形成，保护 NET 导致的肺表面活性物质失活。

炎症期间中性粒细胞胞外陷阱（NET）数量的增加会导致系统功能障碍。然而，抑制 NET 形成 (NETosis) 的宿主蛋白和因子尚未明确确定。在这里，我们发现先天免疫集合素肺表面活性蛋白-D (SP-D) 通过与 LPS 结合来减弱人中性粒细胞中脂多糖 (LPS) 介导的 NETosis。小鼠 SP-D 缺陷 (Sftpd -/-) 会导致 LPS 介导的炎症期间肺部形成过多的 NET。在缺乏 SP-D 的情况下，NET 会抑制肺表面活性剂的表面活性特性，这对于防止肺泡（肺部的呼吸结构）塌陷至关重要。SP-D 逆转 NET 介导的表面活性剂抑制并恢复表面活性剂的生物物理性质。据我们所知，