Autophagy during Mycobacterium tuberculosis infection and implications for future tuberculosis medications

Yu, Xiaoli; Li, Chunmei; Hong, Wang; Pan, Weihua; Xie, Jianping

doi:10.1016/j.cellsig.2013.02.011

Cited by 36 publications

(28 citation statements)

References 31 publications

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“…Although these drugs are strong autophagy inducers, they are also immunosuppressing drugs and therefore their direct use in TB therapies is counterproductive (Ni Cheallaigh et al, 2011;Yu et al, 2013). Nevertheless, direct delivery of these drugs to the lungs using a nanoparticle system to enable specific particle uptake by professional phagocytic cells has been proposed in an attempt to minimize the systemic side effects (Ni Cheallaigh et al, 2011).…”

Section: Arg677trp (C2029t)mentioning

confidence: 99%

Autophagy in the Fight Against Tuberculosis

Bento

Empadinhas

Mendes

2015

DNA and Cell Biology

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Tuberculosis (TB), a chronic infectious disease mainly caused by the tubercle bacillus Mycobacterium tuberculosis, is one of the world's deadliest diseases that has afflicted humanity since ancient times. Although the number of people falling ill with TB each year is declining, its incidence in many developing countries is still a major cause of concern. Upon invading host cells by phagocytosis, M. tuberculosis can replicate within infected cells by arresting the maturation of the phagosome whose function is to target the pathogen for elimination. Host cells have mechanisms of controlling this evasion by inducing autophagy, an elaborate cellular process that targets bacteria for progressive elimination, decreasing bacterial loads within infected cells. In addition, autophagy activation also aids in the control of inflammation, contributing to a more efficient innate immune response against M. tuberculosis. Several innovative TB therapies have been envisaged based on autophagy manipulation, with some of them revealing high potential for future clinical trials and eventual implementation in healthcare systems. Thus, this review highlights the recent advances on the innate immune response regulation by autophagy upon M. tuberculosis infection and the promising new autophagy-based therapies for TB. Mycobacterium tuberculosis: Biology and Infection

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Section: Arg677trp (C2029t)mentioning

confidence: 99%

Autophagy in the Fight Against Tuberculosis

Bento

Empadinhas

Mendes

2015

DNA and Cell Biology

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“…Regarding TLRs, TLR2 is responsible for the recognition of mycobacterial cell wall antigens, while TLR4 recognizes heat shock proteins and TLR9 is activated by mycobacterial DNA (70). The activation TLRs by Mtb infection induces a variety of inflammatory reactions in addition to autophagy (71). Intriguingly, TLR-induced signaling and vitamin D receptor (VDR) signaling synergistically enhance antibacterial autophagy (72).…”

Section: Tuberculosis and Autophagymentioning

confidence: 99%

“…Intriguingly, TLR-induced signaling and vitamin D receptor (VDR) signaling synergistically enhance antibacterial autophagy (72). ROS-induced autophagy has been proposed to be a mechanism for killing intracellular pathogens in macrophages (71), and the "en- (75). Genome-wide siRNA screening to identify host factors associated with the intracellular survival of Mtb in THP-1 cells selected a number of candidates that collectively interfere with autophagy-inducing pathways at multiple points (76).…”

Section: Tuberculosis and Autophagymentioning

confidence: 99%

Autophagy in the Pathogenesis of Pulmonary Disease

2013

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Autophagy is a process of lysosomal self-degradation that helps to maintain the homeostatic balance between the synthesis, degradation and recycling of cellular proteins and organelles. Autophagy does not simply function as the machinery for supplying amino acids in response to energy demands, it is an adaptive pathway of cytoprotection against cellular stressors, including starvation, reactive oxygen species (ROS), endoplasmic reticulum (ER) stress and microbial infection. Accordingly, autophagy is considered to be the mediator of a variety of cellular processes and cell fates, including cell survival and death, cellular senescence and immune responses. Due to the organ-specific role of gas exchange, various cell types within the lungs are serially exposed to a diverse array of cellular stressors, and growing evidence has revealed the crucial involvement of autophagy in the pathogenic processes underlying pulmonary diseases. We herein review recent findings regarding the role of autophagy in cellular processes and cell fates and summarize the role that autophagy appears to play in the pathogenesis of pulmonary diseases.

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“…Mtb infection induces a variety of inflammatory reactions and also induces autophagy [52,53] . Intriguingly, TLR-induced signaling and vitamin D receptor (VDR) signaling synergistically enhance antibacterial autophagy [54] .…”

Section: Autophagymentioning

confidence: 99%

“…Intriguingly, TLR-induced signaling and vitamin D receptor (VDR) signaling synergistically enhance antibacterial autophagy [54] . ROS-induced autophagy has been proposed to be a mechanism for killing of intracellular pathogens in macrophages [53] and the "enhanced intracellular survival" gene of Mtb enhances intracellular survival of Mtb by modulating ROS-dependent autophagy [55] . Therefore, autophagy plays a key regulatory role in clearance of pathogens and autophagy induction by appropriate stimuli can be an ambitious therapeutic option.…”

Section: Autophagymentioning

confidence: 99%

Autophagy and Cellular Senescence in Lung Diseases

Kuwano

Araya

Hara

et al. 2015

Journal of Biochemistry and Molecular Biology Research

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cells. The detailed molecular mechanism for regulation of autophagy and cellular senescence is complex and the role of autophagy and cellular senescence is overlap significantly. We review molecular mechanisms of autophagy and cellular senescence, and summarize the role of autophagy and cellular senescence in pulmonary disease pathogeneses. AUTOPHAGYAutophagy is a process of lysosomal self-degradation that helps maintain homeostatic balance between the synthesis, degradation and recycling of cellular proteins and organelles [1] . At the cellular level, auto-digestion takes place within lysosomes and proteasomes. Proteasomes are involved in the clearance of ubiquitin-conjugated soluble proteins, whereas autophagy delivers diverse cytoplasmic components to the lysosome, including soluble proteins, aggregateprone proteins, and organelles [2] . Autophagy is not simply machinery for amino acid supply in response to energy demand, it is an adaptive pathway of cytoprotection from cellular stresses, involving starvation, reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, and microbe infection [2] . ABSTRACTAutophagy is a process of lysosomal self-degradation that helps maintain homeostatic balance between the synthesis, degradation and recycling of cellular proteins and organelles. In addition to nutrient starvation, a wide array of cellular stresses are also known to be strong inducers of autophagy, indicating that autophagy is not only simple amino acid supply machinery in response to energy demand but also a central component of the integrated stress response for cytoprotection. Since autophagy is an adaptive pathway of cytoprotection from cellular stresses, involving starvation, reactive oxygen species, endoplasmic reticulum stress, and microbe infection, it is reasonable to suggest that autophagy is closely related with aging. Indeed, autophagy diminishes with aging and accelerated aging can be attributed to reduced autophagy. Cellular senescence is also one of the cellular stress responses as well as autophagy, and considered to be one of the processes of aging. Cellular senescence has been widely implicated in disease pathogenesis in terms of not only impaired cell repopulation but also aberrant cytokine secretions of senescence associated secretory phenotype, which may exert deleterious effects on the tissue microenvironment of neighboring

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Autophagy during Mycobacterium tuberculosis infection and implications for future tuberculosis medications

Cited by 36 publications

References 31 publications

Autophagy in the Fight Against Tuberculosis

Autophagy in the Fight Against Tuberculosis

Autophagy in the Pathogenesis of Pulmonary Disease

Autophagy and Cellular Senescence in Lung Diseases

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