Erratum: FIP200 is Involved in Murine <b><i>Pseudomonas</i></b> Infection by Regulating HMGB1 Intracellular Translocation
2017-07-25T13:50:19Z (GMT) by
<b><i>Background: </i></b>FIP200, a critical autophagy initiating protein, can participate in numerous cellular functions including cancer development; however, its functional role in <i>P. aeruginosa</i> infection of alveolar macrophages is unknown. <b><i>Methods: </i></b>To investigate the role of FIP200 in host defense, we transfected murine alveolar macrophage MH-S cells with FIP200 siRNA. Having confirmed that FIP200 knockdown inhibited PAO1-induced autophagosme formation, we sought to characterize the underlying signaling pathways by immunoblotting. Further, we used <i>fip200</i> KO mice to study the effects of <i>fip200</i> deficiency on HMGB1 translocation. <b><i>Results: </i></b>We showed that <i>Pseudomonas</i> PAO1 strain infection facilitated autophagosome formation, whereas knockdown of FIP200 inhibited autophagosome formation and HMGB1 expression in MH-S cells. Silencing FIP200 impaired the translocation of HMGB1 to cytosol of MH-S cells and almost abolished acetylation of HMGB1 during PAO1 infection. In contrast, FIP200 overexpression facilitated the cytosol translocation of HMGB1 from nuclei and increased acetylation of HMGB1 in PAO1-infected MH-S cells. Importantly, expression and acetylation of HMGB1 were also significantly down-regulated in <i>fip200</i> KO mice following PAO1 infection. <b><i>Conclusions: </i></b>Collectively, these findings elucidate that FIP200 may regulate expression and translocation of HMGB1 during PAO1 infection, which may indicate novel therapeutic targets to control pulmonary infection.