Helicobacter pylori upregulates PAD4 expression via stabilising HIF-1α to exacerbate rheumatoid arthritis
Authors' conclusion
Our findings reveal a novel mechanism by which H. pylori infection contributes to RA progression.
Study context
- Population
- Patients with rheumatoid arthritis (RA), H. pylori-negative and H. pylori-positive; MH7A and GES-1 cells
- Comparison
- H. pylori-positive vs H. pylori-negative patients with RA
Main finding
As reported in the abstract
- Disease Activity Score (DAS-28) and anticitrullinated protein antibody (ACPA) levels significantly higher in H. pylori-positive than H. pylori-negative patients with RA
- Polyclonal ACPA from H. pylori-positive patients promoted cell proliferation and induced IL-6 and IL-8 secretion
- H. pylori infection induces cellular protein citrullination by upregulating PAD4
- Direct functional binding of HIF-1α on the PADI4 gene promoter
- PAD4 interacts with and citrullinates keratin 1 (K1); serum and synovial fluid anti-Cit-K1 antibody markedly increased in H. pylori-infected patients with RA
Original publication
Helicobacter pylori upregulates PAD4 expression via stabilising HIF-1α to exacerbate rheumatoid arthritis. Ann Rheum Dis. Published 14 November 2024. doi:10.
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