Effect of CTRP6 Deficiency on LPS-Mediated Acute Inflammatory Response in Mice
XU Ke1,2, GUO Xuemin1, HUANG Xin1,2, JI Miao1,2, ZHENG Cheng2, PENG Yongjia2, TENG Yiqun3, WU Wenjing2*, ZHANG Jin2*
CTRP6 (C1q/TNF-related protein 6) is a novel adipocytokine, which has been proved to be a regulator in animal lipid metabolism, as well as a participant in the body’s inflammatory response. In this study, CTRP6–/– (CTRP6 knockout mice) were used to establish an acute inflammatory model by intraperitoneal injection of LPS (lipopolysaccharide) in order to unveil the effects of CTRP6 deficiency on acute inflammatory response inmice. Firstly, two-month old male CTRP6–/– (KO) mice were randomly divided into two groups (5 mice/group), LPS treatment group and normal saline group, with WT (wild-type) mice as control groups. The analysis of Realtime PCR and ELISA showed that the expression of CTRP6 was down-regulated in various tissues and serum of WT mice with LPS injection, which indicates that the CTRP6 gene is closely related to the acute inflammation induced by LPS. Then, With the comparison of the two genotypes, the inflammatory factors TNF-α and IL-1β in the KO mice were increased less than WT mice with LPS injection. Furthermore, the degree of lung injury was evaluated by tissue section and lung tissue dry-wet ratio analysis. The lung of KO mice showed less inflammatory than that of WT mice with LPS injection. Finally, BMDMs (bone marrow-derived macrophages) from each genotype were treated with LPS and both genotypes showed increased inflammatory factors, while inflammatory factors and NF-κB phosphorylation of CTRP6–/– BMDMs increased less than that of WT BMDMs. In conclusion, CTRP6 gene is closely related to the inflammatory response. CTRP6 deficiency lead to a lower level of acute inflammatory response, then reduce the damage in mice treated with LPS.
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