Abstract
Pathogenic potentials of the gastric pathogen, Helicobacter pylori, have been proposed, evaluated, and confirmed by many laboratories for nearly 4 decades since its serendipitous discovery in 1983 by Barry James Marshall and John Robin Warren. Helicobacter pylori is the first bacterium to be categorized as a definite carcinogen by the International Agency for Research on Cancer (IARC) of the World Health Organization (WHO). Half of the world’s population carries H. pylori, which may be responsible for severe gastric diseases like peptic ulcer and gastric cancer. These two gastric diseases take more than a million lives every year. However, the role of H. pylori as sole pathogen in gastric diseases is heavily debated and remained controversial. It is still not convincingly understood, why most (80–90%) H. pylori infected individuals remain asymptomatic, while some (10–20%) develop such severe gastric diseases. Moreover, several reports indicated that colonization of H. pylori has positive and negative associations with several other gastrointestinal (GI) and non-GI diseases. In this review, we have discussed the state of the art knowledge on “H. pylori factors” and several “other factors,” which have been claimed to have links with severe gastric and duodenal diseases. We conclude that H. pylori infection alone does not satisfy the “necessary and sufficient” condition for developing aggressive clinical outcomes. Rather, the cumulative effect of a number of factors like the virulence proteins of H. pylori, local geography and climate, genetic background and immunity of the host, gastric and intestinal microbiota, and dietary habit and history of medicine usage together determine whether the H. pylori infected person will remain asymptomatic or will develop one of the severe gastric diseases.
Highlights
Two gastric diseases, peptic ulcer (246,700 deaths/year) and gastric cancer (782,685 deaths/year), together are responsible for over a million of global deaths annually (Moraga et al, 2017; Bray et al, 2018)
Helicobacter pylori is a definite carcinogen with proven capabilities to trigger gastric adenocarcinoma and gastric MALT-lymphoma
Only a minor fraction of the people infected with the virulent H. pylori strains develops severe gastric diseases, while most of the infections remain benign indicating involvement of multiple factors
Summary
Peptic ulcer (246,700 deaths/year) and gastric cancer (782,685 deaths/year), together are responsible for over a million of global deaths annually (Moraga et al, 2017; Bray et al, 2018). H. pylori strains with Y58/E59 polymorphism in the CagL carry higher risk for inducing a gastric cancer (Table 2; Yeh et al, 2019). The East-Asian H. pylori strains carry the “D”-type segment in the C-terminal region of the CagA protein, which facilitates stronger CagA-SHP2 interactions and enhanced downstream signaling leading to aggressive gastric diseases (Higashi et al, 2002; Figure 2).
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