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Differential inflammatory response to Helicobacter pylori infection: etiology and clinical outcomes

Authors White J, Winter J, Robinson K

Received 20 May 2015

Accepted for publication 10 July 2015

Published 13 August 2015 Volume 2015:8 Pages 137—147

DOI https://doi.org/10.2147/JIR.S64888

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Juan Pablo de Rivero Vaccari

Peer reviewer comments 2

Editor who approved publication: Dr Ning Quan

Jonathan Richard White,1 Jody Anne Winter,2 Karen Robinson1

1NIHR Biomedical Research Unit in Gastrointestinal and Liver Diseases at Nottingham University Hospitals NHS Trust and The University of Nottingham, Nottingham, 2Interdisciplinary Biomedical Research Centre, School of Science and Technology, Nottingham Trent University, Nottingham, UK

Abstract: The bacterial pathogen Helicobacter pylori commonly colonizes the human gastric mucosa during early childhood and persists throughout life. The organism has evolved multiple mechanisms for evading clearance by the immune system and, despite inducing inflammation in the stomach, the majority of infections are asymptomatic. H. pylori is the leading cause of peptic ulcer disease and gastric cancer. However, disease outcomes are related to the pattern and severity of chronic inflammation in the gastric mucosa, which in turn is influenced by both bacterial and host factors. Despite over 2 decades of intensive research, there remains an incomplete understanding of the circumstances leading to disease development, due to the fascinating complexity of the host–pathogen interactions. There is accumulating data concerning the virulence factors associated with increased risk of disease, and the majority of these have pro-inflammatory activities. Despite this, only a small proportion of those infected with virulent strains develop disease. Several H. pylori virulence factors have multiple effects on different cell types, including the induction of pro- and anti-inflammatory, immune stimulatory, and immune modulatory responses. The expression of multiple virulence factors is also often linked, making it difficult to assess the meaning of their effects in isolation. Overall, H. pylori is thought to usually modulate inflammation and limit acute damage to the mucosa, enabling the bacteria to persist. If this delicate balance is disturbed, disease may then develop.

Keywords: Helicobacter pylori, inflammation, mucosal immunity, peptic ulcer disease, gastric cancer

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