Abstract
Autophagy is an evolutionary conserved intracellular process whereby cells break down long-lived proteins and organelles. Accumulating evidences suggest increasing physiological significance of autophagy in pathogenesis of infectious diseases. Anthrax lethal toxin (LT) exerts its influence on numerous cells and herein, we report a novel effect of LT-induced autophagy on mammalian cells. Several autophagy biochemical markers including LC3-II conversion, increased punctuate distribution of GFP-LC3 and development of acidic vesicular organelles (AVO) were detected in cells treated with LT. Analysis of individual LT component revealed a moderate increase in LC3-II conversion for protective antigen-treated cells, whereas the LC3-II level in lethal factor-treated cells remained unchanged. In addition, our preliminary findings suggest a protective role of autophagy in LT intoxication as autophagy inhibition resulted in accelerated cell death. This study presents a hitherto undescribed effect of LT-induced autophagy on cells and provides the groundwork for future studies on the implication of autophagy in anthrax pathogenesis.
Highlights
Autophagy is an intracellular process whereby cells break down long-lived proteins and organelles and is morphologically characterized by the formation of many large autophagic vacuoles in cytoplasm [1]
Our study has provided evidence that autophagy was involved in anthrax pathogenesis
LT is recognized as a critical virulence factor in B. anthracis pathogenesis
Summary
Autophagy is an intracellular process whereby cells break down long-lived proteins and organelles and is morphologically characterized by the formation of many large autophagic vacuoles in cytoplasm [1]. This evolutionary process is conserved across all eukaryotic cells and is fundamentally important in normal and pathological cell physiology and development [2, 3]. The process of autophagy begins with the formation of isolation membrane or phagophore followed by sequestration of organelles or part of the cytoplasm to form autophagosome. Cytosolic form of LC3-I is processed into a lipidated LC3-II which is tightly associated with autophagosome membranes [8]. LF is a potent inhibitor on many functions of immune cells such as macrophages, dendritic cells, neutrophils, T cells and B cells [14]
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