Autophagy is an evolutionarily conserved process in eukaryotic cells which involves catabolic degradation of organelles and cytosolic components in autophagosomes to generate needed amino acids to maintain cellular homeostasis during various stress conditions. The formation of autophagosomes is dependent on autophagy-related proteins (ATGs) which interact with endosome trafficking proteins such as Rab GTPases. Autophagy is also a critical innate immune defense mechanism against invading intracellular pathogens that results in pathogen destruction in autolysosomes after lysosomal fusion. Paradoxically, many of these pathogens developed evasive mechanisms to avoid autophagosomes and the degradative environment of autolysosomes. These include pathogenic Mycobacteria, Salmonella, Listeria, Ehrlichia, Anaplasma, Shigella, Chlamydia, Franciscella and many others that interact with or evade the autophagy pathway within the phagocytic cells. For example, Mycobacterium tuberculosis secretes N-acetyl transferase, Eis, among others to impede autophagy. Listeria avoids autophagic recognition by coating itself with host proteins such as actin. Mycobacteria, Listeria, Helicobacter all seem to regulate host autophagy through the modulation of microRNA targeting autophagy. Salmonella and Ehrlichia interfere with the lysosome biogenesis by maintaining a phosphorylated TFEB. In contrast, other bacterial pathogens, such as Coxiella, use autophagy machinery to replicate.
Although autophagy is an intrinsic process in mammalian cells, immune cells such as macrophages, dendritic cells, neutrophils which interact with or are targets of bacterial pathogens utilize autophagy-dependent mechanisms to combat pathogens.
This Research Topic is therefore focused on illuminating molecular mechanisms involved in autophagy-mediated elimination of bacteria and those developed by pathogens to exploit, inhibit or manipulate autophagy within dendritic cells, macrophages, and neutrophils. Submission of Original Research articles, Reviews, and Mini-Reviews are encouraged on the following topics:
• Bacterial pathogen recognition and elimination by autophagy.
• Mechanisms of infection enhancement involving autophagy.
• Bacterial mechanisms to evade or exploit autophagy
• Regulation of inflammation and immunity to bacterial pathogens via autophagy.
• Non-canonical autophagy pathways (LC3-associated phagocytosis and others).
• Autophagy-based therapy
Autophagy is an evolutionarily conserved process in eukaryotic cells which involves catabolic degradation of organelles and cytosolic components in autophagosomes to generate needed amino acids to maintain cellular homeostasis during various stress conditions. The formation of autophagosomes is dependent on autophagy-related proteins (ATGs) which interact with endosome trafficking proteins such as Rab GTPases. Autophagy is also a critical innate immune defense mechanism against invading intracellular pathogens that results in pathogen destruction in autolysosomes after lysosomal fusion. Paradoxically, many of these pathogens developed evasive mechanisms to avoid autophagosomes and the degradative environment of autolysosomes. These include pathogenic Mycobacteria, Salmonella, Listeria, Ehrlichia, Anaplasma, Shigella, Chlamydia, Franciscella and many others that interact with or evade the autophagy pathway within the phagocytic cells. For example, Mycobacterium tuberculosis secretes N-acetyl transferase, Eis, among others to impede autophagy. Listeria avoids autophagic recognition by coating itself with host proteins such as actin. Mycobacteria, Listeria, Helicobacter all seem to regulate host autophagy through the modulation of microRNA targeting autophagy. Salmonella and Ehrlichia interfere with the lysosome biogenesis by maintaining a phosphorylated TFEB. In contrast, other bacterial pathogens, such as Coxiella, use autophagy machinery to replicate.
Although autophagy is an intrinsic process in mammalian cells, immune cells such as macrophages, dendritic cells, neutrophils which interact with or are targets of bacterial pathogens utilize autophagy-dependent mechanisms to combat pathogens.
This Research Topic is therefore focused on illuminating molecular mechanisms involved in autophagy-mediated elimination of bacteria and those developed by pathogens to exploit, inhibit or manipulate autophagy within dendritic cells, macrophages, and neutrophils. Submission of Original Research articles, Reviews, and Mini-Reviews are encouraged on the following topics:
• Bacterial pathogen recognition and elimination by autophagy.
• Mechanisms of infection enhancement involving autophagy.
• Bacterial mechanisms to evade or exploit autophagy
• Regulation of inflammation and immunity to bacterial pathogens via autophagy.
• Non-canonical autophagy pathways (LC3-associated phagocytosis and others).
• Autophagy-based therapy