Role of the Helicobacter pylori‐Induced inflammatory response in the development of gastric cancer1. Issue 3 (22nd January 2013)

• Record Type: Journal Article
• Authors: Lamb, Acacia; Chen, Lin‐Feng
• Is Part Of: Journal of cellular biochemistry. Volume 114:Issue 3(2013:Mar.)
• Page Start: 491
• Page End: 497
• Publication Date: 2013-01-22
• Subjects: Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.24389
• Languages: English
• ISSNs: 0730-2312

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <p> <italic>Helicobacter pylori</italic> (<italic>H. pylori</italic>) infection causes chronic gastritis and peptic ulceration and is the strongest risk factor for the development of gastric cancer. The pathogenesis of <italic>H. pylori</italic> is believed to be associated with infection‐initiated chronic gastritis, which is characterized by enhanced expression of many inflammatory genes. <italic>H. pylori</italic> 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 <italic>H. pylori</italic> 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 <italic>H. pylori</italic>‐induced inflammation. J. Cell. Biochem. 114: 491–497, 2013. © 2012 Wiley Periodicals, Inc.</p> </abstract>