▪ How is H. pylori targeted by the host autophagy machinery?
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▪ Which ligands on H. pylori initiate autophagy?
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▪ Is ubiquitin involved in the ‘marking’ of H. pylori ligand(s) for the autophagic machinery?
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▪ Does H. pylori-induced autophagy stimulate the autophagic degradation of cellular organelles?
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▪ Does H. pylori-induced autophagy follow a canonical or noncanonical pathway?
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▪ Does H. pylori induce LAP instead of, or in conjunction with, canonical autophagy?
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▪ Considering that VacA has a crucial role in H. pylori-associated autophagy, what is the detailed mechanism of VacA-mediated autophagy?
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▪ What role does the channel-forming activity of VacA play in autophagy induction and modulation of autophagic flux?
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▪ What role do the other virulence factors of H. pylori play in H. pylori-associated autophagy?
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▪ Do TLR4 and/or NOD2 play any role in H. pylori-induced autophagy?
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▪ Is there any relationship between NOD polymorphism and H. pylori-associated autophagy?
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▪ Do host autophagic processes contribute to the persistence and antibiotic resistance of H. pylori?
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| ▪ How are host autophagic processes related to altered immune responses during infection? |
