Objective:To investigate the impact and possible regulatory mechanism of triggering receptor ex-pressed on myeloid cells 2(TREM2)in lung ischemia-reperfusion injury(LIRI).Methods:Twelve male C57BL/6J wild-type mice(WT)and twelve TREM2 knockout mice(TREM2 KO)were randomly divided into four groups:WT micesham operation group(WT group),TREM2 KO mice sham operation group(TREM2 KO group),WT mice LIRI group(WT+LIRI group)and TREM2 KO mice LIRI group(TREM2 KO+LIRI group),with 6 mice in each group.The mouse LIRI model was prepared by occluding the hilum of the left lung for 1 h and reperfusion for 24 h in the WT+LIRI group and TREM2 KO+LIRI group,while only the hilum of the lung-was opened without occluding in the chest.Western blotting,immunofluorescence,reverse transcription-quantita-tive PCR(RT-qPCR),hematoxylin-eosin(HE)staining,and lung tissue wet-to-dry weight(W/D)ratio were per-formed to evaluate the impact of TREM2 knockout on tissue injury,inflammation and macrophage pyroptosis af-ter lung ischemia-reperfusion in mice.Results:Knockout of TREM2 significantly exacerbated morphological changes in lung tissue after LIRI,increased lung injury scores(P＜0.05),elevated the W/D ratio of lung tissue(P＜0.05),promoted the expression of inflammatory factors interleukin-1β(IL-1β)and IL-18 in lung tissue after LIRI(P＜0.05),and enhanced the expression of macrophage pyroptosis markers cysteine aspartic acid-specific protease-1(caspase-1)and pore-forming protein Gasdermin-D(GSDMD)in lung tissue after LIRI(P＜0.05).Conclusion:TREM2 knockout can exacerbate LIRI,and its mechanism may be related to caspase-1-mediated py-roptosis of lung macrophages induced by the loss of TREM2.
维普
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