Dual effects of <i>Helicobacter pylori</i> vacuolating cytotoxin on human eosinophil apoptosis in early and late periods of stimulation

Kim, Jung Mogg; Kim, Joosung; Lee, Jin Young; Sim, Young Suk; Kim, Young Jeon; Oh, Yu‐Kyoung; Yoon, Ho Joo; Kang, Jae Seon; Youn, Jeehee; Kim, Nayoung; Jung, Hyun Chae; Kim, Sunil

doi:10.1002/eji.200939882

Cited by 22 publications

(24 citation statements)

References 53 publications

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“…Eosinophils were isolated from peripheral blood of volunteers using a magnetic cell separation system (Miltenyi Biotec, Bergisch Gladbach, Germany), as described previously . The Hanyang University College of Medicine Review Board approved the protocol used to obtain blood from volunteers.…”

Section: Methodsmentioning

confidence: 99%

The Flavone Eupatilin Inhibits Eotaxin Expression in an NF‐κB‐Dependent and STAT6‐Independent Manner

Jeon

Kim

et al. 2015

Scand J Immunol

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The CC chemokine eotaxin contributes to epithelium-induced inflammation in airway diseases such as asthma. Eupatilin (5,7-dihydroxy-3 0 ,4 0 ,6 0 -trimethoxyflavone), a bioactive component of Artemisia asiatica Nakai (Asteraceae), is reported to inhibit the adhesion of eosinophils to bronchial epithelial cells. However, little is known about the molecular mechanism of eupatilin-induced attenuation of bronchial epithelium-induced inflammation. In this study, we investigated the effect of eupatilin on expression of eotaxin-1 (CCL11), a potent chemoattractant for eosinophils. Eupatilin significantly inhibited eotaxin expression in bronchial epithelial cells stimulated with TNF-a, while NF-jB and IjBa kinase (IKK) activities declined concurrently. Eupatilin also inhibited mitogen-activated protein kinase (MAPK) activity; however, all of these antiinflammatory activities were reversed by MAPK overexpression. In contrast, eupatilin did not affect the signal transducer and activator of transcription 6 (STAT6) signalling in bronchial epithelial cells stimulated with IL-4. Furthermore, eupatilin significantly attenuated TNF-a-induced eosinophil migration. These results suggest that the eupatilin inhibits the signalling of MAPK, IKK, NF-jB and eotaxin-1 in bronchial epithelial cells, leading to inhibition of eosinophil migration.

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Section: Methodsmentioning

confidence: 99%

The Flavone Eupatilin Inhibits Eotaxin Expression in an NF‐κB‐Dependent and STAT6‐Independent Manner

Jeon

Kim

et al. 2015

Scand J Immunol

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“…Although vacuolization notably affects the homeostasis of endosomal-lysosomal organelles, it is not the cause of VacA-induced cell death [194–196]. VacA induces apoptosis through its action on mitochondria, autophagy and connexin 43 (Cx43) turnover [174, 179, 194, 196–199].…”

Section: Vacuolization and Unknown Cell Death Pathwaysmentioning

confidence: 99%

“…VacA induces apoptosis through its action on mitochondria, autophagy and connexin 43 (Cx43) turnover [174, 179, 194, 196–199]. VacA effect on mitochondria relies on the formation of anion-selective channels in the inner mitochondrial membrane, whose activity decreases the transmembrane potential [200].…”

Section: Vacuolization and Unknown Cell Death Pathwaysmentioning

confidence: 99%

Cytoplasmic vacuolization in cell death and survival

et al. 2016

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Cytoplasmic vacuolization (also called cytoplasmic vacuolation) is a well-known morphological phenomenon observed in mammalian cells after exposure to bacterial or viral pathogens as well as to various natural and artificial low-molecular-weight compounds. Vacuolization often accompanies cell death; however, its role in cell death processes remains unclear. This can be attributed to studying vacuolization at the level of morphology for many years. At the same time, new data on the molecular mechanisms of the vacuole formation and structure have become available. In addition, numerous examples of the association between vacuolization and previously unknown cell death types have been reported. Here, we review these data to make a deeper insight into the role of cytoplasmic vacuolization in cell death and survival.

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“…Concerning the mechanistic relation of ion channel formation in the mitochondrial inner membrane to subsequent apoptosis, essentially three points have been clarified: (i) Import of VacA causes loss of the mitochondrial membrane potential [5,25,85], (ii) members of the Bcl-2 family, including Bax and Bak are intrinsically involved in VacA-dependent apoptosis [5,26,29,30,91,95], and (iii) cytochrome c and other mitochondrial proteins are released into the cytosol [5,26,29,31,85]. …”

Section: The Mechanism Of Cytochrome C Release: Vaca and Apoptosismentioning

confidence: 99%

Helicobacter pylori vacuolating toxin A and apoptosis

Rassow

2011

Cell Communication and Signaling

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VacA, the vacuolating cytotoxin A of Helicobacter pylori, induces apoptosis in epithelial cells of the gastic mucosa and in leukocytes. VacA is released by the bacteria as a protein of 88 kDa. At the outer surface of host cells, it binds to the sphingomyelin of lipid rafts. At least partially, binding to the cells is facilitated by different receptor proteins. VacA is internalized by a clathrin-independent mechanism and initially accumulates in GPI-anchored proteins-enriched early endosomal compartments. Together with early endosomes, VacA is distributed inside the cells. Most of the VacA is eventually contained in the membranes of vacuoles. VacA assembles in hexameric oligomers forming an anion channel of low conductivity with a preference for chloride ions. In parallel, a significant fraction of VacA can be transferred from endosomes to mitochondria in a process involving direct endosome-mitochondria juxtaposition. Inside the mitochondria, VacA accumulates in the mitochondrial inner membrane, probably forming similar chloride channels as observed in the vacuoles. Import into mitochondria is mediated by the hydrophobic N-terminus of VacA. Apoptosis is triggered by loss of the mitochondrial membrane potential, recruitment of Bax and Bak, and release of cytochrome c.

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Dual effects of Helicobacter pylori vacuolating cytotoxin on human eosinophil apoptosis in early and late periods of stimulation

Cited by 22 publications

References 53 publications

The Flavone Eupatilin Inhibits Eotaxin Expression in an NF‐κB‐Dependent and STAT6‐Independent Manner

The Flavone Eupatilin Inhibits Eotaxin Expression in an NF‐κB‐Dependent and STAT6‐Independent Manner

Cytoplasmic vacuolization in cell death and survival

Helicobacter pylori vacuolating toxin A and apoptosis

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