Four types of <i><scp>B</scp>ifidobacteria</i> trigger autophagy response in intestinal epithelial cells

Lin, Rong; Jiang, Ye; Zhao, Xin; Yang, Guan; Qian, Wei; Fu, Xiao Chao; Ren, Hun Yu; Hou, Xiao Hua

doi:10.1111/1751-2980.12179

Cited by 29 publications

(17 citation statements)

References 45 publications

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“…These include effects by the microbiota on autophagy (Lin et al, 2014), a cellular recycling process that is genetically linked to PD risk, and when impaired may lead to reduced clearance of αSyn aggregates (Beilina and Cookson, 2015; Nalls et al, 2014). Additionally, intestinal bacteria have been shown to modulate proteasome function (Cleynen et al, 2014), which may also aid in the clearance of αSyn inclusions.…”

Section: Discussionmentioning

confidence: 99%

Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease

Sampson

Debelius

Thron

et al. 2016

Cell

2,717

2,193

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Summary The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. However, a functional link between gut bacteria and neurodegenerative diseases remains unexplored. Synucleinopathies are characterized by aggregation of the protein α-synuclein (αSyn), often resulting in motor dysfunction as exemplified by Parkinson's disease (PD). Using mice that overexpress αSyn, we report herein that gut microbiota are required for motor deficits, microglia activation, and αSyn pathology. Antibiotic treatment ameliorates, while microbial re-colonization promotes, pathophysiology in adult animals, suggesting postnatal signaling between the gut and the brain modulates disease. Indeed, oral administration of specific microbial metabolites to germ-free mice promotes neuroinflammation and motor symptoms. Remarkably, colonization of αSyn-overexpressing mice with microbiota from PD patients enhances physical impairments compared to microbiota transplants from healthy human donors. These findings reveal that gut bacteria regulate movement disorders in mice, and suggest that alterations in the human microbiome represent a risk factor for PD.

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Section: Discussionmentioning

confidence: 99%

Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease

Sampson

Debelius

Thron

et al. 2016

Cell

2,717

2,193

View full text Add to dashboard Cite

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“…Irving et al (2014) demonstrated that peptidoglycan derived from Helicobacter pylori and Pseudomonas aeruginosa promotes autophagy in epithelial cells via NOD1 receptor activation. Moreover, several studies reported potential of some Bifidobacteria and Lactobacillus species to stimulate or suppress autophagy (Wu et al, 2013; Lin et al, 2014; Motevaseli et al, 2016). …”

Section: Introductionmentioning

confidence: 99%

Lactobacillus fermentum Postbiotic-induced Autophagy as Potential Approach for Treatment of Acetaminophen Hepatotoxicity

et al. 2017

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The aim of this study was to investigate the potential of postbiotics originated from Lactobacillus fermentum BGHV110 strain (HV110) to counteract acetaminophen (APAP)-induced hepatotoxicity in HepG2 cells. This strain was selected according to its autophagy inducing potential, based on previous studies reporting protective role of autophagy in APAP caused cellular damage. Cell viability was assessed using MTT and LDH assays, while autophagy was monitored by qPCR analysis of BECN1, Atg5, p62/SQSTM1, and PINK1 mRNA expression and by Western blot analysis of p62/SQSTM1 and lipidated LC3 accumulation. Our results showed that detrimental effect of APAP on cell viability was suppressed in the presence of HV110 which was linked with increased conversion of LC3 protein and p62/SQSTM1 protein degradation. Additionally, higher p62/SQSTM1 and PINK1 mRNA transcription were noticed in cells co-treated with APAP/HV110, simultaneously. In conclusion, this study suggests that HV110 enhances activation of PINK1-dependent autophagy in HepG2 cells and its eventual co-supplementation with APAP could be potentially used for alleviation of hepatotoxic side effects caused by APAP overdose.

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“…Indeed, single nucleotide polymorphisms (SNPs) within two autophagy-related genes, autophagy-related 16-like 1 (ATG16L1) and the immunity-related GTPase family M (IRGM), are important loci for IBD pathogenesis [12,13]. Dysfunction of these autophagy-related proteins is associated with survival of intracellular bacteria, pro-inflammatory cytokine secretion, and colitis onset [12,14]. Thus, controlling how autophagy is regulated might be a critical strategy for IBD prevention and therapy.…”

Section: Introductionmentioning

confidence: 99%

The Role of Probiotics in Lipopolysaccharide-Induced Autophagy in Intestinal Epithelial Cells

Han

Zhang

Shi

et al. 2016

Cell Physiol Biochem

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Background/Aims: Dysfunction of autophagy has been associated with loss of intestinal homeostasis. Lipopolysaccharide (LPS) from Gram-negative bacteria is known to be a major initiator of intestinal epithelial cell (IEC) autophagy. Although probiotics have been recognized to be involved in many therapeutic properties and participate in host defense responses, the molecular mechanisms by which probiotics exert these positive effects remain unknown. This study assessed the effect of probiotics on LPS-induced physical barrier dysfunction and the underlying mechanism of probiotic action in IECs with a focus on autophagy. Methods: A LPS-induced autophagic model was established in rat IEC18 cells wherein cells were treated with culture medium supernatants of Bifidobacteria following LPS intervention at indicated times. Autophagosomes in IEC18 cells were visualized by confocal microscopy after transfection with a tandem GFP-mCherry-LC3 construct and also by transmission electron microscopy. Autophagy-associated protein levels were analyzed by western blot and transepithelial electrical resistance (TEER) was measured using an epithelial voltohmmeter. Results: Probiotic treatment could effectively inhibit LPS-induced autophagy, as evidenced by the decreased ratio of microtubule-associated light chain 3 (LC3)-II/LC3-I, fewer autophagic vacuoles, and reduced punctate distribution of GFP-mCherry-LC3. In addition, probiotics prevented chloroquine (CQ) inhibition of autophagic flux and autophagolysosomal fusion as indicated by a failure to recruit LAMP1 and cathepsin D to lysosomes. Interestingly, ATG16L1 knockdown did not inhibit the effect of probiotics on LPS-induced autophagy. Furthermore, the diminished barrier function could be prevented by probiotics. Conclusions: We provide evidence that autophagy mediation by probiotics may be involved in enteroprotection against LPS-induced intestinal epithelial toxicity, and could serve as a novel mechanism through which probiotics promote and maintain gut homeostasis.

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Four types of Bifidobacteria trigger autophagy response in intestinal epithelial cells

Abstract: Bifidobacteria initiate autophagy activation in IEC. The Atg12-Atg5-Atg16 multimeric complex might participate in the activation of Bifidobacteria-induced cell autophagy.

Cited by 29 publications

References 45 publications

Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease

Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease

Lactobacillus fermentum Postbiotic-induced Autophagy as Potential Approach for Treatment of Acetaminophen Hepatotoxicity

The Role of Probiotics in Lipopolysaccharide-Induced Autophagy in Intestinal Epithelial Cells

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