• Title/Summary/Keyword: VacA toxin

Search Result 5, Processing Time 0.019 seconds

Inhibitory Effect of Ponciretin on Helicobacter pylori VacA Toxin-induced Vacuolation in HeLa Cells

  • KIM JONG-MI;SHIN JI-EUN;BAE EUN-AH;HAN MYUNG JOO;KIM DONG-HYUN
    • Journal of Microbiology and Biotechnology
    • /
    • v.16 no.1
    • /
    • pp.46-51
    • /
    • 2006
  • The inhibitory effects of flavanone derivatives on Helicobacter pylori (HP) growth, infection and VacA toxininduced vacuolation were investigated. Among flavanones tested, ponciretin potently inhibited the growth of HP with a MIC value of 0.01 mg/ml and VacA toxin-induced vacuolation in HeLa cells with $IC_{50}$ value of 0.078 mM. However, other flavanones inhibited neither HP growth nor VacA toxininduced vacuolation. All flavanones tested did not inhibit HP infection to KATO III cells. Ponciretin also inhibited activation of procaspase-3 to caspase-3 in HeLa cell induced by HP VacA toxin, but did not affect Bax and Bcl-2 protein levels. These findings indicate that ponciretin inhibits growth as well as vacuolation by HP VacA toxin, which induces cell death via proteolytic activation of a cascade of caspases.

Helicobacter pylori Vacuolating Toxin Exhibits Polar Activity of $Cl^-$ Secretion and Secretory Response to Carbachol in T84 Cells

  • Jin, Nan-Ge;Jin, Yong-Ri;So, In-Suk;Kim, Ki-Whan
    • The Korean Journal of Physiology and Pharmacology
    • /
    • v.8 no.5
    • /
    • pp.289-293
    • /
    • 2004
  • To investigate whether VacA (vacuolating toxin) produced by Helicobacter pylori Korean stain 99 induces intestinal secretion, purified VacA was added to T84 cell monolayers mounted in Ussing chambers, and electrical parameters were monitored. Mucosal addition of low pH-pretreated VacA increased short circuit current (Isc). The effect was time- and dose-dependent and saturable. The time-to-peak Isc was concentration-dependent. Chloride channel inhibitors, niflumic acid or 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB), inhibited VacA-stimulated Isc. Carbachol (CCh)-induced increase of Isc was prolonged by the addition of VacA to the mucosal side only. The effect was unaltered by the addition of niflumic acid. VacA did not show cytopathic effects. These studies indicate that VacA is a nonlethal toxin that acts in a polar manner on T84 monolayers to potentiate $Cl^-$ secretion and the response to CCh secretion without decrease in monolayer resistance. VacA may contribute to diarrhea diseases in human intestinal epithelial cells.

Inhibitory Effect of Ginseng Polyacetylenes on Infection and Vacuolation of Helicobacter pylori

  • Kim, Jong-Mi;Shin, Ji-Eun;Han, Myung-Joo;Baek, Nam-In;Kim, Dong-Hyun
    • Natural Product Sciences
    • /
    • v.9 no.3
    • /
    • pp.158-160
    • /
    • 2003
  • Polyacetylenes were isolated from Panax ginseng C.A. Meyer (Family Araliaceae), and their inhibitory effects on growth, infection and VacA vacuolation of Helicobacter pylori (HP) were investigated. Ginseng polyacetylenes did not inhibit the infection of HP into KATO cells. However, polyacetylenes inhibited HP growth and vacuolation of Hela by VacA toxin. Panaxytriol showed the most potent inhibition with $IC_{50}$ values of 0.05 and 0.046 mg/ml, respectively.

Inhibitory Effect of Ginseng Saponins and Polysaccharides on Infection and Vacuolation of Helicobacter pylori

  • Kim, Jong-Mi;Shln, Ji-Eun;Han, Myung-Joo;Park, Sung-Hwan;Kim, Dong-Hyun
    • Journal of Microbiology and Biotechnology
    • /
    • v.13 no.5
    • /
    • pp.706-709
    • /
    • 2003
  • Ginsenosides and polysaccharides were isolated from Panax ginseng C.A. Meyer (Family Araliaceae) by treating at low ($60^{\circ}C$, LT), mild ($100^{\circ}C$, MT), and high ($120^{\circ}C$, HT) temperatures, and their inhibitory effects on growth, infection, and VacA vacuolation of Helicobacter pylori (HP) were investigated. The molecular weights of polysaccharides decreased as the processing temperature increased. Ginseng polysaccharides inhibited the HP infection into KATO III cells, but did not inhibit growth of HP and VacA vacuolation of HeLa cells. HT polysaccharides showed the most potent inhibition with $IC_50$ value of 6.8 mg/ml. Ginseng saponins did not inhibit the infection of HP into KATO cells. However, 20(s)-protopanaxadiol showed the most potent inhibition of HP growth and vacuolation of HeLa by VacA toxin with $IC_50$ values of 0.05 and 0.067 mg/ml, respectively.

Increased Risk of Severe Gastric Symptoms by Virulence Factors vacAs1c, alpA, babA2, and hopZ in Helicobacter pylori Infection

  • Lee, Dong-Hae;Ha, Jong-Hun;Shin, Jeong-Ih;Kim, Kyu-Min;Choi, Jeong-gyu;Park, Seorin;Park, Jin-Sik;Seo, Ji-Hyeun;Park, Ji-Shook;Shin, Min-Kyoung;Baik, Seung-Chul;Lee, Woo-Kon;Youn, Hee-Shang;Cho, Myung-Je;Kang, Hyung-Lyun;Jung, Myunghwan
    • Journal of Microbiology and Biotechnology
    • /
    • v.31 no.3
    • /
    • pp.368-379
    • /
    • 2021
  • Two virulence factors of Helicobacter pylori, cagA and vacA, have been known to play a role in the development of severe gastric symptoms. However, they are not always associated with peptic ulcer or gastric cancer. To predict the disease outcome more accurately, it is necessary to understand the risk of severe symptoms linked to other virulence factors. Several other virulence factors of H. pylori have also been reported to be associated with disease outcomes, although there are many controversial descriptions. H. pylori isolates from Koreans may be useful in evaluating the relevance of other virulence factors to clinical symptoms of gastric diseases because the majority of Koreans are infected by toxigenic strains of H. pylori bearing cagA and vacA. In this study, a total of 116 H. pylori strains from Korean patients with chronic gastritis, peptic ulcers, and gastric cancers were genotyped. The presence of virulence factors vacAs1c, alpA, babA2, hopZ, and the extremely strong vacuolating toxin was found to contribute significantly to the development of severe gastric symptoms. The genotype combination vacAs1c/alpA/babA2 was the most predictable determinant for the development of severe symptoms, and the presence of babA2 was found to be the most critical factor. This study provides important information on the virulence factors that contribute to the development of severe gastric symptoms and will assist in predicting clinical disease outcomes due to H. pylori infection.