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Mammalian intestinal intracellular Microsporidia subvert host cell autophagy to promote replication

Intracellular pathogens such as Microsporidia can interact with host proteostasis pathways such as autophagy. Previous work done in Caenorhabditis elegans demonstrated involvement of autophagy in controlling Microsporidia proliferation through ubiquitin labelling of the parasite and subsequent degradation by autophagolysomes. However, it remains unknown if such mechanisms also play the role in mammalian models. Here we used immunochemistry assays, super-resolution confocal imaging, chemical and genetic modulation of the autophagy flux to elucidate the interplay between autophagy and Microsporidia in mammalian cells. We show that despite targeting by early autophagy markers (ubiquitin and p62); the host cell was not able to complete autophagy-mediated removal of Encephalitozoon cuniculi. Furthermore, instead of helping to control Microsporidia proliferation, the induction of autophagy dramatically increased proliferation of two microsporidia species in two different mammalian cell models. Finally, we showed that the reduction of the autophagy flux using siRNA treatment or microbiota-derived metabolites was able to reduce the parasite proliferation. Taken together our results indicate that Microsporidia infecting mammalian cells developed strategies to evade the host autophagy and, in contrast, can divert the autophagy flux to promote their own growth.