Effects of transcription factor activator protein-1 on interleukin-8 expression and enteritis in response to Clostridium difficile toxin A

Lee, Jin Young; Park, Hyeri; Oh, Yu‐Kyoung; Kim, Yeong-Jeon; Youn, Jeehee; Han, Joong‐Soo; Kim, Jung Mogg

doi:10.1007/s00109-007-0237-7

Cited by 36 publications

(37 citation statements)

References 46 publications

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“…following kinase inhibitors: PD98059 (an inhibitor of MEK1/2), SB203580 (an inhibitor of p38), and SP600125 (an inhibitor of JNK) [26,27]. The results indicated that pretreatment with SB203580 significantly attenuated Bax expression in mitochondrial fractions from VacA-stimulated eosinophils.…”

Section: H Pylori Vaca Induces Mitochondrial Trafficking Of Activatementioning

confidence: 95%

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

Kim

Lee

et al. 2010

Eur J Immunol

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Although Helicobacter pylori infections of the gastric mucosa are characterized by the infiltration of inflammatory cells such as eosinophils, the responses of eosinophils to H. pylori vacuolating cytotoxin (VacA) have not been fully elucidated. This study investigates the role of VacA in the apoptosis of human eosinophils. We treated human eosinophils with purified H. pylori VacA and observed that induction of apoptosis is a relatively late event. Expression of cellular inhibitor of apoptosis protein (c-IAP)-2 was upregulated during the early period of VacA stimulation, and transfection with c-IAP2 siRNA augmented apoptotic cell death. VacA caused the translocation of cytoplasmic Bax to the mitochondria and increased cytochrome c release from mitochondria in eosinophils. Transfection of an EoL-1 eosinophil cell line with Bax siRNA decreased the release of cytochrome c and DNA fragmentation. Furthermore, apoptosis facilitated by Bax and cytochrome c was primarily regulated by p38 MAPK in VacA-treated eosinophils. These results suggest that the exposure of human eosinophils to H. pylori VacA induces the early upregulation of c-IAP2 and a relatively late apoptotic response, with the apoptosis progressing through a sequential pathway that includes p38 MAPK activation, Bax translocation, and cytochrome c release.

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Section: H Pylori Vaca Induces Mitochondrial Trafficking Of Activatementioning

confidence: 95%

“…Luciferase assay was performed in accordance with the manufacture's instructions (Tropix, Bedford, MA, USA) [14,21]. Recombinant adenovirus containing a dominant-negative p38a mutant (ADV-105) was obtained from Cell Biolabs (San Diego, CA, USA) [26].…”

Section: Transfectionmentioning

confidence: 99%

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

Kim

Lee

et al. 2010

Eur J Immunol

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“…26,28,35,36 The study was approved by the Ethics Committee of Seoul National University Hospital. After the surgical specimens were washed twice in HBSS, the epithelia were removed by scraping the surface with a glass slide.…”

Section: Isolation Of Primary Human Intestinal Epithelial Cellsmentioning

confidence: 99%

Bacteroides fragilis enterotoxin upregulates lipocalin-2 expression in intestinal epithelial cells

Yoo

Jung

et al. 2013

Laboratory Investigation

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Enterotoxigenic Bacteroides fragilis (ETBF) produces an B20 kDa B. fragilis enterotoxin (BFT), which plays an essential role in mucosal inflammation. Lipocalin (Lcn)-2, a siderophore-binding antimicrobial protein, is critical for control of bacterial infection; however, expression of Lcn-2 in BFT-exposed intestinal epithelial cells has not been elucidated. In the present study, stimulation of human intestinal epithelial cells with BFT resulted in the upregulation of Lcn-2 expression that was a relatively late response of intestinal epithelial cells compared with human b-defensin (hBD)-2 expression. The upregulation of Lcn-2 was dependent on AP-1 but not on NF-kB signaling. Lcn-2 induction via AP-1 was regulated by mitogenactivated protein kinases (MAPKs) including ERK and p38. Lcn-2 was secreted from the apical and basolateral surfaces in BFT-treated cells. These results suggest that a signaling pathway involving MAPKs and AP-1 is required for Lcn-2 induction in intestinal epithelial cells exposed to BFT, after which the secreted Lcn-2 may facilitate antimicrobial activity within ETBF-infected mucosa.

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“…Recombinant adenovirus containing a dominantnegative p38a mutant (ADV-105) was obtained from Cell Biolabs, Inc (San Diego, CA). Transfection with adenovirus was performed as described previously [39].…”

Section: Plasmids Transfection and Luciferase Assaymentioning

confidence: 99%

Inhibition of apoptosis in Bacteroides fragilis enterotoxin‐stimulated intestinal epithelial cells through the induction of c‐IAP‐2

2008

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Enterotoxigenic Bacteroides fragilis produces an approximately 20-kDa heat-labile enterotoxin (BFT) that plays an essential role in generating mucosal inflammation. Although it is well known that proinflammatory signals are expressed in BFT-stimulated intestinal epithelial cells, cell death processes have not been elucidated. BFT induced apoptosis in HT-29 cells, but the apoptosis was first apparent 36 h after stimulation. During the early period of BFT stimulation, expression of cellular inhibitor of apoptosis protein-2 (c-IAP2) increased, and inhibition of c-IAP2 augmented the apoptotic cell death. Inhibition of BFT-induced COX-2 expression decreased prostaglandin E 2 (PGE 2 ) production, which led not only to a decrease of c-IAP2 activity but also to an enhancement of DNA fragmentation in the early period of BFT stimulation. Furthermore, apoptosis inhibition through PGE 2 and c-IAP2 was mainly regulated by a p38 mitogen-activated protein kinase (MAPK). These results suggest that the inhibition of apoptosis may be mediated by a sequential pathway, including MAPK, COX-2, PGE 2 and c-IAP2, in the early period of stimulation. The delay in the onset of epithelial cell apoptosis after enterotoxigenic B. fragilis infection may be important to the host since it can provides sufficient time for epithelial cells to generate signals for the activation of mucosal inflammation and it may increase the chances of bacterial colonization.

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Effects of transcription factor activator protein-1 on interleukin-8 expression and enteritis in response to Clostridium difficile toxin A

Cited by 36 publications

References 46 publications

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

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

Bacteroides fragilis enterotoxin upregulates lipocalin-2 expression in intestinal epithelial cells

Inhibition of apoptosis in Bacteroides fragilis enterotoxin‐stimulated intestinal epithelial cells through the induction of c‐IAP‐2

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