How Helicobacter pylori Infection Affects Rheumatoid Arthritis
Author Information
Author(s): Wu Hui, Yuan Hanmei, Zhang Jin, He Taojun, Deng Yilin, Chen Ying, Zhang Yunqi, Chen Weisan, Wu Chao
Primary Institution: The Eighth Affiliated Hospital of Sun Yat-Sen University, Shenzhen, Guangdong, China
Hypothesis
This study aimed to investigate the underlying pathogenic mechanism of H. pylori infection in the progression of rheumatoid arthritis (RA).
Conclusion
H. pylori infection contributes to RA progression by upregulating PAD4, which citrullinates keratin 1, leading to increased levels of anti-Cit-K1 antibodies.
Supporting Evidence
- H. pylori-positive patients with RA had significantly higher DAS-28 and ACPA levels than H. pylori-negative patients.
- ACPA from H. pylori-positive patients promoted cell proliferation and secretion of inflammatory factors.
- H. pylori infection was found to induce cellular protein citrullination by upregulating PAD4.
- PAD4 was shown to interact with and citrullinate keratin 1 (K1).
- Serum levels of anti-Cit-K1 antibody were markedly increased in H. pylori-infected patients with RA.
Takeaway
H. pylori, a common stomach bacteria, can make rheumatoid arthritis worse by changing how the body reacts to certain proteins.
Methodology
The study compared Disease Activity Score (DAS-28) and serum anticitrullinated protein antibody (ACPA) levels between H. pylori-negative and H. pylori-positive RA patients, and used various assays to explore the molecular mechanisms.
Limitations
The specific locations of PAD4-dependent citrullination on K1 remain unidentified, and the study was limited to a single sample for synovial membrane analysis.
Participant Demographics
Patients with rheumatoid arthritis, including 39 H. pylori-positive and 42 H. pylori-negative individuals.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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