6 Questions
What is the mechanism by which H. pylori modifies its LPS to evade immune detection?
H. pylori alters the O antigens of its LPS to mimic Lewis Y and X antigens of gastric epithelia.
How does the VacA toxin of H. pylori contribute to the disruption of the epithelial barrier?
VacA induces pro-inflammatory signaling when in the nucleus, triggers the release of cytochrome C from the mitochondria, leading to cell death and disrupting the epithelial barrier.
What is the role of the T4SS in H. pylori's virulence?
The T4SS injects peptidoglycan to promote inflammation via IL-8 production.
How do H. pylori's OMVs contribute to the induction of inflammation?
OMVs enter cells via lipid rafts and induce inflammation via NOD1 signaling.
What is the role of adhesins BabA and SabA in H. pylori's virulence?
Adhesins BabA and SabA mediate strong binding to epithelial Le antigens, upregulated during inflammation.
How does H. pylori's urease enzyme contribute to its survival in the stomach?
Urease helps the bacterium survive in the acidic stomach environment.
Study Notes
Helicobacter pylori
- Gram-negative, commensal bacterium that causes chronic gastritis and peptic ulcers.
- Resides in the crypts of the stomach, and chronic gastritis can lead to gastric cancer in 1% of patients.
Virulence Factors
- Urease: helps the bacterium survive in the acidic stomach environment.
- Adhesins BabA and SabA: mediate strong binding to epithelial Le antigens, upregulated during inflammation.
- Modified LPS and flagella: block immune detection by altering O antigens to mimic Lewis Y and X antigens of gastric epithelia.
- T4SS (Type IV Secretion System): injects peptidoglycan to promote inflammation via IL-8 production.
- VacA: induces pro-inflammatory signalling when in the nucleus, triggers the release of cytochrome C from the mitochondria, leading to cell death and disrupting the epithelial barrier.
Immune Evasion and Disruption
- Disrupts the epithelial barrier, allowing the bacterium to pass through tight junctions.
- Localizes on T cells and inhibits their activation and proliferation.
- Releases OMVs (Outer Membrane Vesicles) that enter cells via lipid rafts and induce inflammation via NOD1 signalling.
This quiz covers the mechanisms of Helicobacter pylori infections, including evasion of immune detection and virulence factors such as urease that enable it to survive in the stomach.
Make Your Own Quizzes and Flashcards
Convert your notes into interactive study material.
Get started for free
