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

Phagocytosis of Candida albicans Inhibits Autophagic Flux in Macrophages