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<p>Cytotoxic-associated gene A (CagA) is a key virulence factor of <i>Helicobacter pylori</i>, associated with gastric ulcers and stomach cancer. The bacterium employs a Cag-type IV secretion system for translocation of CagA into the host cells. This study investigates the impact of CagA antibodies on CagA translocation into gastric epithelial cells in vitro. Our findings reveal that CagA synthesis and translocation across bacterial membranes is a continuous process initiated upon host-cell contact. Notably, the treatment of&#xa0;<i>Helicobacter pylori</i>&#xa0;with CagA-specific antibodies significantly inhibited the translocation of CagA into host cells during infection. These results suggest that the CagA antibody may serve as a potential therapeutic strategy to combat&#xa0;<i>Helicobacter pylori</i>&#xa0;pathogenesis. A similar result was obtained when CagT antibody was used under the same conditions. Notably, the CagT antibody exhibited a more pronounced pathoblocking effect, likely due to its accessibility on the bacterial surface as a structural component of Cag-T4SS. Taken together, this study provides insights into the therapeutic potential of CagA and CagT antibodies to mitigate&#xa0;<i>Helicobacter pylori</i>&#xa0;infection, while also advancing our understanding of the mechanisms involved in CagA translocation across the bacterial membranes to the host cell.</p>

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Helicobacter pylori CagA and CagT antibodies arrest the translocation of CagA into gastric epithelial cells

  • 期刊论文

  • 发表日期：

    2025年5月20日

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  • Swagata Sain,
  • Bhawna Solanki,
  • Navin Kumar

摘要

Cytotoxic-associated gene A (CagA) is a key virulence factor of Helicobacter pylori, associated with gastric ulcers and stomach cancer. The bacterium employs a Cag-type IV secretion system for translocation of CagA into the host cells. This study investigates the impact of CagA antibodies on CagA translocation into gastric epithelial cells in vitro. Our findings reveal that CagA synthesis and translocation across bacterial membranes is a continuous process initiated upon host-cell contact. Notably, the treatment of Helicobacter pylori with CagA-specific antibodies significantly inhibited the translocation of CagA into host cells during infection. These results suggest that the CagA antibody may serve as a potential therapeutic strategy to combat Helicobacter pylori pathogenesis. A similar result was obtained when CagT antibody was used under the same conditions. Notably, the CagT antibody exhibited a more pronounced pathoblocking effect, likely due to its accessibility on the bacterial surface as a structural component of Cag-T4SS. Taken together, this study provides insights into the therapeutic potential of CagA and CagT antibodies to mitigate Helicobacter pylori infection, while also advancing our understanding of the mechanisms involved in CagA translocation across the bacterial membranes to the host cell.