Abstract:
:The Helicobacter pylori immunodominant protein, CagA, is associated with severe gastritis and carcinoma. Injection of CagA into gastric epithelial cells by type IV secretion leads to actin-cytoskeletal rearrangements and cell scattering. CagA has been reported to have no role in the induction of transcription factor NF-kappaB and IL-8, which are crucial determinants for chronic inflammation. Here, we provide several lines of evidence showing that CagA is able to induce IL-8 in a time- and strain-dependent manner. We also show that by exchanging specific cagA genes, high IL-8-inducing H. pylori strains could be converted into low inducing strains and vice versa. Our results suggest that IL-8 release induced by CagA occurs via a Ras-->Raf-->Mek-->Erk-->NF-kappaB signaling pathway in a Shp-2- and c-Met-independent manner. Thus, CagA is a multifunctional protein capable of effecting both actin remodeling and potentiation of chemokine release.
journal_name
Proc Natl Acad Sci U S Aauthors
Brandt S,Kwok T,Hartig R,König W,Backert Sdoi
10.1073/pnas.0409873102keywords:
subject
Has Abstractpub_date
2005-06-28 00:00:00pages
9300-5issue
26eissn
0027-8424issn
1091-6490pii
0409873102journal_volume
102pub_type
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