Abstract
Cellular homeostasis requires the balanced regulation of anabolic and catabolic processes. While anabolic metabolism consumes energy to build up cellular components, catabolic processes break down organic matters in order to provide energy for the cell and its anabolic processes. Autophagy is a highly conserved and regulated catabolic process by which the eukaryotic cell degrades unnecessary, undesirable, or dysfunctional cellular components, including organelles (1–3). Autophagy is induced by a variety of extra-and intracellular stress stimuli, such as nutrient starvation, oxidative stress, or accumulation of damaged organelles or toxic protein aggregates. Initiation of autophagy first leads to the formation of cup-shaped structures known as phagophores that engulf the undesirable or damaged cellular components. Subsequent elongation of phagophores form double-membrane vesicles called autophagosomes, which deliver their cargo to lysosomes where the content is degraded and recycled (1–3). Autophagy plays a central role in quality control of organelles and proteins, and additionally is a key mechanism to maintain cellular energy levels and nutrient homeostasis during starvation, promoting the recycling and salvage of cellular nutrients. Furthermore, the cellular autophagic machinery is also used to remove invading intracellular pathogens, a process called xenophagy (1, 2). In this case, phagophores engulf invading microbes forming autophagosomes and steering them toward lysosomal degradation. Thus, xenophagy is an innate immune mechanism against bacterial infection that has been shown to be essential to restrict intracellular growth of many bacteria such as Salmonella enterica serovar Typhimurium (4), Mycobacterium tuberculosis (5, 6), Listeria monocytogenes (7), or Group A Streptococcus (8).
Highlights
Reviewed by: Eric Ghigo, Centre national de la recherche scientifique, France Robert Heinzen, National Institutes of Health, USA Soubeyran Philippe, Institut national de la santé et de la recherche médicale, France
While anabolic metabolism consumes energy to build up cellular components, catabolic processes break down organic matters in order to provide energy for the cell and its anabolic processes
Detection of bacterial components in the cytoplasm of mammalian cells induces autophagy via the activation of toll-like receptor 4 (TLR4) by bacterial lipopolysaccharide (LPS) and recognition of bacterial peptidoglycan by NOD1 and NOD2 [9, 10]
Summary
Reviewed by: Eric Ghigo, Centre national de la recherche scientifique, France Robert Heinzen, National Institutes of Health, USA Soubeyran Philippe, Institut national de la santé et de la recherche médicale, France. Recruitment of autophagy proteins to the phagosome, such as the ULK1 complex, Beclin1, and ATG16L1, initiates membrane nucleation of the phagophore that will engulf the intracellular bacteria [10,11,12] (Figure 1B). The attachment of syntaxin 17 to the autophagosomal membrane enables the fusion with lysosomes and represents the final maturation step of autophagosomes into autolysosomes [13] (Figure 1E), which normally leads to bacterial degradation in case of infection-induced autophagy [2].
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