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Early Molecular Events in Murine Gastric Epithelial Cells Mediated by Helicobacter pylori CagA
Author(s) -
Banerjee Aditi,
Basu Malini,
Blanchard Thomas G.,
Chintalacharuvu Subba R.,
Guang Wei,
Lillehoj Erik P.,
Czinn Steven J.
Publication year - 2016
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/hel.12300
Subject(s) - caga , helicobacter pylori , helicobacter , microbiology and biotechnology , biology , immunology , gene , genetics , virulence
Background Murine models of Helicobacter pylori infection are used to study host–pathogen interactions, but lack of severe gastritis in this model has limited its usefulness in studying pathogenesis. We compared the murine gastric epithelial cell line GSM 06 to the human gastric epithelial AGS cell line to determine whether similar events occur when cultured with H. pylori . Materials and Methods The lysates of cells infected with H. pylori isolates or an isogenic cagA ‐deficient mutant were assessed for translocation and phosphorylation of CagA and for activation of stress pathway kinases by immunoblot. Results Phosphorylated CagA was detected in both cell lines within 60 minutes. Phospho‐ ERK 1/2 was present within several minutes and distinctly present in GSM 06 cells at 60 minutes. Similar results were obtained for phospho‐ JNK , although the 54 kD a phosphoprotein signal was dominant in AGS , whereas the lower molecular weight band was dominant in GSM 06 cells. Conclusion These results demonstrate that early events in H. pylori pathogenesis occur within mouse epithelial cells similar to human cells and therefore support the use of the mouse model for the study of acute CagA‐associated host cell responses. These results also indicate that reduced disease in H. pylori ‐infected mice may be due to lack of the Cag PAI , or by differences in the mouse response downstream of the initial activation events.