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Autophagy machinery has roles in the defense against microorganisms such as . Lipidated LC3, the marker protein of autophagy, participates in the elimination of by forming a single-membrane phagosome; this process is called LC3-associated phagocytosis (LAP). However, the influence of on autophagic flux is not clear. In this study, we found that inhibited LC3 turnover in macrophages. After the phagocytosis of in macrophages, we observed fewer acridine orange-positive vacuoles and RFP-GFP-LC3 puncta without colocalization with phagocytized . However, phagocytosis of led to LC3 recruitment, but p62 and ATG9A did not colocalize with LC3 or . These effects are due to an MTOR-independent pathway. Nevertheless, we found that the pattern-associated molecular pattern -glucan increased LC3 turnover. In addition, phagocytosis of caused a decrease in BrdU incorporation. Blocking autophagic flux aggravated this effect. Our findings suggest that phagocytosis of decreases autophagic flux but induces LAP in an MTOR-independent manner in macrophages. Occupation of LC3 by recruiting engulfed might contribute to the inhibition of autophagic flux. Our study highlights the coordinated machinery between canonical autophagy and LAP that defends against challenge.
Authors : Duan Zhimin , Chen Qing , Du Leilei , Tong Jianbo , Xu Song , Zeng Rong , Ma Yuting , Chen Xu , Li Min ,
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