NOD1 is required forHelicobacter pyloriinduction of IL-33 responses in gastric epithelial cells

• DOI: 10.1111/cmi.12826
• Publication Date: 2018-02-02T09:22:45Z
• Authors: Le Son Tran; Darren Tran; Amanda De Paoli; Kimberley D'Costa; Sarah J. Creed; Garrett Z. Ng; Lena Le; Philip Sutton; J. Silke; U. Nachbur; Richard L. Ferrero
• Keywords: NOD1; CagA

Helicobacter pylori (H. pylori) causes chronic inflammation which is a key precursor to gastric carcinogenesis. It has been suggested that H. may limit this immunopathology by inducing the production of interleukin 33 (IL-33) in epithelial cells, thus promoting T helper 2 immune responses. The molecular mechanism underlying IL-33 response infection, however, remains unknown. In study, we demonstrate activates signalling via pathogen recognition molecule Nucleotide-Binding Oligomerisation Domain-Containing Protein 1 (NOD1) and its adaptor protein receptor-interacting serine–threonine Kinase 2, promote both full-length processed cells. Furthermore, responses were dependent on actions Type IV secretion system, required for activation NOD1 pathway, as well system effector protein, CagA. Importantly, Nod1+/+ mice with infection exhibited significantly increased splenic IL-13 responses, but decreased IFN-γ when compared Nod1−/− animals. Collectively, our data identify an important regulator mucosal infection. We suggest play role protection against excessive inflammation.