Autophagy protects type II alveolar epithelial cells from Mycobacterium tuberculosis infection

Guo, Xia; Ji, Tianxing; Yong, Xia; Ma, Yue

doi:10.1016/j.bbrc.2013.01.111

Cited by 22 publications

(22 citation statements)

References 27 publications

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“…Autophagic processes can also contribute to tolerance mechanisms, that confer protection to the host by minimizing damage caused by the infection [35,36]. In particular, membrane damage and/or pore-forming toxins induce classic starvation responses, by triggering signals dedicated to maintenance of energy and nutrient homeostasis, that may explain recovery of the host cells from sublethal attack [37][38][39][40][41]. In oyster and clam hemocytes, V. tapetis extracellular products (ECPs) induced loss of adherence and inhibition of phagocytosis [42 and references quoted therein].…”

Section: Discussionmentioning

confidence: 99%

Autophagic processes in Mytilus galloprovincialis hemocytes: Effects of Vibrio tapetis

Balbi

Cortese

Ciacci

et al. 2018

Fish & Shellfish Immunology

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Section: Discussionmentioning

confidence: 99%

Autophagic processes in Mytilus galloprovincialis hemocytes: Effects of Vibrio tapetis

Balbi

Cortese

Ciacci

et al. 2018

Fish & Shellfish Immunology

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“…The growth of intracellular bacteria can be restricted by autophagy, either canonical or non-canonical, in which ATG5 is essential. Mycobacterium tuberculosis is one of the pathogens in vacuoles that is eliminated by autophagy ( 77 ) and a double membrane structure was observed in tuberculosis infected type II alveolar epithelial cells ( 78 ). Atg5 knockout mice presented with a heavier M. tuberculosis burden, more severe inflammation, and higher levels of IL-1 ( 79 ).…”

Section: Atg5 In Immunity Regulationmentioning

confidence: 99%

Exploring the Role of Autophagy-Related Gene 5 (ATG5) Yields Important Insights Into Autophagy in Autoimmune/Autoinflammatory Diseases

2018

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Autophagy is a highly conserved process that degrades certain intracellular contents in both physiological and pathological conditions. Autophagy-related proteins (ATG) are key players in this pathway, among which ATG5 is indispensable in both canonical and non-canonical autophagy. Recent studies demonstrate that ATG5 modulates the immune system and crosstalks with apoptosis. However, our knowledge of the pathogenesis and regulatory mechanisms of autophagy in various immune related diseases is lacking. Thus, a deeper understanding of ATG5's role in the autophagy mechanism may shed light on the link between autophagy and the immune response, and lead to the development of new therapies for autoimmune diseases and autoinflammatory diseases. In this focused review, we discuss the latest insights into the role of ATG5 in autoimmunity. Although these studies are at a relatively early stage, ATG5 may eventually come to be regarded as a “guardian of immune integrity.” Notably, accumulating evidence indicates that other ATG genes may have similar functions.

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“…In addition, induction of autophagy in A549 presents a protective role against Mtb infection. Mtb could cause further necrosis among LC3-silenced A549 than that among wild-type A549 (Guo et al, 2013 ). Therefore, autophagy maybe the main mechanism that defends against invasion of pathogen (Li et al, 2012 ; Thurston et al, 2012 ; Wileman, 2013 ).…”

Section: Introductionmentioning

confidence: 99%

Heparin-binding Hemagglutinin of Mycobacterium tuberculosis Is an Inhibitor of Autophagy

Zheng

Zhou

et al. 2017

Front. Cell. Infect. Microbiol.

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Airway epithelial cell is often the initial site of attack by pathogens, and cell death is commonly caused by internalization of Mycobacterium tuberculosis (Mtb). However, the mechanism of interaction between epithelial cells and Mtb is not well understood. In this study, we investigated the role of the heparin-binding hemagglutinin (HBHA) protein of Mtb in the function of epithelial cells. In particular, the autophagy of A549 cells was determined based on microtubule-associated protein 1 light chain 3 alpha (LC3) activity. Autophagosome formation was detected by Monodansylcadaverine (MDC) staining and immune fluorescence staining of LC3. Autophagy could be significantly suppressed by HBHA protein. In addition, the LDH assay results showed that HBHA treatment could induce death on A549 cells. To explore the form of cell death, we detected the activity of caspase-3 and LDH release of A549 cells in the presence or absence of caspase inhibitor Z-VAD-FMK. Results demonstrated that HBHA treatment could induce apoptosis of A549 cells. To further confirm these results, we constructed the recombinant Mycobacterium smegmatis (MS) expressing HBHA (rMS-HBHA) and explored the influence of rMS-HBHA on the function of A549 cells. rMS-HBHA infection significantly inhibited LC3 expression and the maturation of autophagosomes in A549 cells. Subsequently, we infected A549 cells with MS and detected the viability of intracellular MS by CFU counts. rMS-HBHA showed higher survival and replication capacity in A549 cells than those of the wild-type MS. Finally, infection of A549 cells with rMS-HBHA caused further apoptosis. These findings suggested that rMS-HBHA could inhibit autophagy, promote its survival and replication within A549 cells, and subsequently induce apoptosis on infected cells to facilitate infection.

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Autophagy protects type II alveolar epithelial cells from Mycobacterium tuberculosis infection

Cited by 22 publications

References 27 publications

Autophagic processes in Mytilus galloprovincialis hemocytes: Effects of Vibrio tapetis

Autophagic processes in Mytilus galloprovincialis hemocytes: Effects of Vibrio tapetis

Exploring the Role of Autophagy-Related Gene 5 (ATG5) Yields Important Insights Into Autophagy in Autoimmune/Autoinflammatory Diseases

Heparin-binding Hemagglutinin of Mycobacterium tuberculosis Is an Inhibitor of Autophagy

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