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Role of the Helicobacter pylori ‐Induced inflammatory response in the development of gastric cancer
Author(s) -
Lamb Acacia,
Chen LinFeng
Publication year - 2013
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24389
Subject(s) - helicobacter pylori , inflammation , chronic gastritis , pathogenesis , gastritis , cancer , immunology , transcription factor , pathogen , virulence factor , gastric mucosa , peptic , virulence , biology , medicine , cancer research , gene , peptic ulcer , stomach , genetics
Helicobacter pylori ( H. pylori ) infection causes chronic gastritis and peptic ulceration and is the strongest risk factor for the development of gastric cancer. The pathogenesis of H. pylori is believed to be associated with infection‐initiated chronic gastritis, which is characterized by enhanced expression of many inflammatory genes. H. pylori utilizes various virulence factors, targeting different cellular proteins, to modulate the host inflammatory response. In this review, we explore the many different ways by which H. pylori initiates inflammation, leveling many “hits” on the gastric mucosa which can lead to the development of cancer. We also discuss some recent findings in understanding the pathogen‐host interactions and the role of transcription factor NF‐κB in H. pylori ‐induced inflammation. J. Cell. Biochem. 114: 491–497, 2013. © 2012 Wiley Periodicals, Inc.