Restoration of heat shock protein70 suppresses gastric mucosal inducible nitric oxide synthase expression induced by <b><i>Helicobacter pylori</i></b>

Yeo, Myoung-Souk; Park, Hyun-kyung; Kim, Dong Kyu; Cho, Sung Won; Kim, Young Suk; Cho, Sang Yun; Paik, Young‐Ki; Hahm, Ki‐Baik

doi:10.1002/pmic.200400951

Cited by 52 publications

(38 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…H. pylori major toxic factors CagA and VacA could induce an increment in many proinflammatory cytokines, such as IL-1␤, TNF-␣, and COX-2 (30-32). In addition, the activation of iNOS, which occurs mainly in macrophages, triggers the generation of a large amount of nitric oxide and thus induces chronic gastritis (33). The present study showed that PA could effectively inhibit gastritis induced by H. pylori by inhibiting IL-1␤, TNF-␣, COX-2, and iNOS gene expression.…”

Section: Discussionmentioning

confidence: 59%

In VitroandIn VivoAntibacterial Activities of Patchouli Alcohol, a Naturally Occurring Tricyclic Sesquiterpene, against Helicobacter pylori Infection

Lian

Chen

et al. 2017

Antimicrob Agents Chemother

View full text Add to dashboard Cite

This study further evaluated the in vitro and in vivo anti-Helicobacter pylori activities and potential underlying mechanism of patchouli alcohol (PA), a tricyclic sesquiterpene. In the in vitro assay, the capacities of PA to inhibit and kill H. pylori were tested on three standard strains at different pH values and on 12 clinical isolates. The effects of PA on H. pylori adhesion (and its alpA, alpB, and babA genes), motility (and its flaA and flaB genes), ultrastructure, and flagellation were investigated. Moreover, the H. pylori resistance to and postantibiotic effect (PAE) of PA were determined. Furthermore, the in vivo effects of PA on H. pylori eradication and gastritis were examined. Results showed that MICs of PA against three standard strains (pH 5.3 to 9) and 12 clinical isolates were 25 to 75 and 12.5 to 50 g/ml, respectively. The killing kinetics of PA were time and concentration dependent, and its minimal bactericidal concentrations (MBCs) were 25 to 75 g/ml. In addition, H. pylori adhesion, motility, ultrastructure, and flagellation were significantly suppressed. PA also remarkably inhibited the expression of adhesion genes (alpA and alpB) and motility genes (flaA and flaB). Furthermore, PA treatment caused a longer PAE and less bacterial resistance than clarithromycin and metronidazole. The in vivo study showed that PA can effectively eradicate H. pylori, inhibit gastritis, and suppress the expression of inflammatory mediators (COX-2, interleukin 1␤, tumor necrosis factor alpha, and inducible nitric oxide synthase [iNOS]). In conclusion, PA can efficiently kill H. pylori, interfere with its infection process, and attenuate gastritis with less bacterial resistance, making it a potential candidate for new drug development.

show abstract

Section: Discussionmentioning

confidence: 59%

In VitroandIn VivoAntibacterial Activities of Patchouli Alcohol, a Naturally Occurring Tricyclic Sesquiterpene, against Helicobacter pylori Infection

Lian

Chen

et al. 2017

Antimicrob Agents Chemother

View full text Add to dashboard Cite

show abstract

“…CXCL8 induction provided a positive control for robustness of infection, n = 3 adenocarcinoma cell line AGS with H. pylori strain P12. A number of previous studies have reported repression of host HSP expression upon H. pylori infection (Axsen et al 2009;Baek et al 2004;Konturek et al 2001;Pierzchalski et al 2006;Targosz et al 2006;Yeo et al 2004). This study is the first to report this effect using the H. pylori strain P12 in AGS cells.…”

Section: Discussionmentioning

confidence: 99%

“…The gastric pathogen H. pylori, the primary cause of chronic gastritis, peptic ulcer, MALT, and gastric cancer, has been demonstrated to down-modulate host-cell HSP expression upon infection (Axsen et al 2009;Baek et al 2004;Konturek et al 2001;Pierzchalski et al 2006;Targosz et al 2006;Yeo et al 2004). The mechanism of H. pylori-mediated host HSP repression is currently unknown, the elucidation of which may provide novel insight into host-pathogen interactions and may prove valuable in the effort to develop anti-HSP strategies for cancer treatment.…”

Section: Discussionmentioning

confidence: 99%

“…Given that CagA is one of the major virulence factors of H. pylori and the sole known protein delivered by the cagPAIencoded T4SS into the host cell during infection, we investigated the importance of CagA for the altered HSP expression previously observed upon H. pylori infection in vitro (Axsen et al 2009;Baek et al 2004;Konturek et al 2001;Pierzchalski et al 2006;Targosz et al 2006;Yeo et al 2004). Wild-type H. pylori strain P12 (P12wt) and its CagAdeficient isogenic mutant (P12ΔcagA) were used to infect the gastric adenocarcinoma cell line AGS to model H. pylori infection of gastric epithelia in vitro (Backert et al 2001;Kwok et al 2002;Kwok et al 2007).…”

Section: H Pylori-mediated Repression Of Host Hsps Expression Is Cagmentioning

confidence: 99%

“…In contrast to the upregulation of host-cell HSP expression associated with such bacterial infections, the gastric pathogen, Helicobacter pylori, has a novel ability to down-modulate host HSP expression upon acute infection of gastric epithelial cells (Axsen et al 2009;Baek et al 2004;Konturek et al 2001;Pierzchalski et al 2006;Targosz et al 2006;Yeo et al 2004). H. pylori is a Gram-negative, spiral bacterium that infects 50 % of humans globally.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The Helicobacter pylori cytotoxin CagA is essential for suppressing host heat shock protein expression

Lang

Gorrell

Tafreshi

et al. 2016

Cell Stress and Chaperones

View full text Add to dashboard Cite

Bacterial infections typically elicit a strong Heat Shock Response (HSR) in host cells. However, the gastric pathogen Helicobacter pylori has the unique ability to repress this response, the mechanism of which has yet to be elucidated. This study sought to characterize the underlying mechanisms by which H. pylori down-modulates host HSP expression upon infection. Examination of isogenic mutant strains of H. pylori defective in components of the type IV secretion system (T4SS), identified the secretion substrate, CagA, to be essential for down-modulation of the HSPs HSPH1 (HSP105), HSPA1A (HSP72), and HSPD1 (HSP60) upon infection of the AGS gastric adenocarcinoma cell line. Ectopic expression of CagA by transient transfection was insufficient to repress HSP expression in AGS or HEK293T cells, suggesting that additional H. pylori factors are required for HSP repression. RT-qPCR analysis of HSP gene expression in AGS cells infected with wild-type H. pylori or isogenic cagA-deletion mutant found no significant change to account for reduced HSP levels. In summary, this study identified CagA to be an essential bacterial factor for H. pylori-mediated suppression of host HSP expression. The novel finding that HSPH1 is down-modulated by H. pylori further highlights the unique ability of H. pylori to repress the HSR within host cells. Elucidation of the mechanism by which H. pylori achieves HSP repression may prove to be beneficial in the identification of novel mechanisms to inhibit the HSR pathway and provide further insight into the interactions between H. pylori and the host gastric epithelium.

show abstract

Current awareness on comparative and functional genomics

2005

Comp Funct Genom

View full text Add to dashboard Cite

In order to keep subscribers up-to-date with the latest developments in their field, this current awareness service is provided by John Wiley & Sons and contains newly-published material on comparative and functional genomics. Each bibliography is divided into 16 sections. I Reviews & symposia; 2 General; 3 Large-scale sequencing and mapping; 4 Evolutionary genomics; 5 Comparative genomics; 6 Pathways, gene families and regulons; 7 Pharmacogenomics; 8 EST, cDNA and other clone resources; 9 Functional genomics; I0 Transcriptomics; II Proteomics; I2 Protein structural genomics; I3 Metabolomics; I4 Genomic approaches to development; I5 Technological advances; I6 Bioinformatics. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted.

show abstract

Restoration of heat shock protein70 suppresses gastric mucosal inducible nitric oxide synthase expression induced by Helicobacter pylori

Cited by 52 publications

References 30 publications

In VitroandIn VivoAntibacterial Activities of Patchouli Alcohol, a Naturally Occurring Tricyclic Sesquiterpene, against Helicobacter pylori Infection

In VitroandIn VivoAntibacterial Activities of Patchouli Alcohol, a Naturally Occurring Tricyclic Sesquiterpene, against Helicobacter pylori Infection

The Helicobacter pylori cytotoxin CagA is essential for suppressing host heat shock protein expression

Current awareness on comparative and functional genomics

Contact Info

Product

Resources

About