Laboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Center for Genomic Medicine, Rigshospitalet, Copenhagen University Hospital, Blegdamsvej 9, DK-2100, Copenhagen, Denmark.
Sci Rep. 2017 Jun 20;7(1):3852. doi: 10.1038/s41598-017-04121-w.
Ficolins are a family of pattern recognition molecules that are capable of activating the lectin pathway of complement. A limited number of reports have demonstrated a protective role of ficolins in animal models of infection. In addition, an immune modulatory role of ficolins has been suggested. Yet, the contribution of ficolins to inflammatory disease processes remains elusive. To address this, we investigated ficolin deficient mice during a lipopolysaccharide (LPS)-induced model of systemic inflammation. Although murine serum ficolin was shown to bind LPS in vitro, there was no difference between wildtype and ficolin deficient mice in morbidity and mortality by LPS-induced inflammation. Moreover, there was no difference between wildtype and ficolin deficient mice in the inflammatory cytokine profiles after LPS challenge. These findings were substantiated by microarray analysis revealing an unaltered spleen transcriptome profile in ficolin deficient mice compared to wildtype mice. Collectively, results from this study demonstrate that ficolins are not involved in host response to LPS-induced systemic inflammation.
纤维胶凝蛋白是一类模式识别分子，能够激活补体的凝集素途径。少数报道表明纤维胶凝蛋白在感染的动物模型中具有保护作用。此外，纤维胶凝蛋白还具有免疫调节作用。然而，纤维胶凝蛋白对炎症性疾病过程的贡献仍然难以捉摸。为了解决这个问题，我们在脂多糖（LPS）诱导的全身炎症模型中研究了纤维胶凝蛋白缺陷小鼠。尽管体外实验表明鼠血清纤维胶凝蛋白能够与 LPS 结合，但 LPS 诱导的炎症在野生型和纤维胶凝蛋白缺陷型小鼠之间在发病率和死亡率方面没有差异。此外，在 LPS 刺激后，野生型和纤维胶凝蛋白缺陷型小鼠之间的炎症细胞因子谱也没有差异。这些发现通过微阵列分析得到了证实，与野生型小鼠相比，纤维胶凝蛋白缺陷型小鼠的脾脏转录组谱没有改变。总的来说，这项研究的结果表明，纤维胶凝蛋白不参与宿主对 LPS 诱导的全身炎症的反应。
