Helicobacter pylori colonizes human gastric mucosa. Its infection
is associated with gastric diseases including gastric
cancer. CagA is one of the most important toxins produced
by H. pylori. It is related to gastric cancer which can be injected
into host cells via a type IV secretion system (T4SS).
CagL is a structural component of T4SS apparatus, which
triggers host cell signaling pathway. It has been reported that
CagL polymorphisms may influence the severity of disease
development. To explore the contribution of CagL polymorphisms
between East Asian and Western H. pylori in pathogenesis,
cagL gene in G27 H. pylori was swapped by K74 cagL
which is identical to East Asian CagL consensus sequence and
by Western 26695 H. pylori, resulting in G27ΔcagL/cagLK74
and G27ΔcagL/cagL26695, respectively. Intriguingly, G27ΔcagL/
cagLK74 showed significantly less ability of IL-8 induction
than G27ΔcagL/cagL26695 while displayed similar abilities of
CagA phosphorylation, and cell elongation. Taken together,
this study suggests that the CagL polymorphism may influence
IL-8 induction, and K74 CagL has less ability to induce
IL-8 secretion than G27 or 26695 CagL. Further research
should address how the different capabilities of IL-8 induction
between intraspecies-CagL are associated with the large
differences of the incidence of gastric cancer between East
Asian and Western countries.
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Roles of the components of the
cag
-pathogenicity island encoded type IV secretion system in
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