Journal
FRONTIERS IN MICROBIOLOGY
Volume 12, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fmicb.2021.713955
Keywords
gastric cancer and peptic ulcer; Helicobacter pylori; other factors; clinical outcomes; inconsistancy
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Funding
- Department of Biotechnology (DBT), Government of India [MED/2017/46]
- Science and Engineering Research Board (SERB) of Department of Science and Technology (DST), Government of India [ECR/2016/171]
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Helicobacter pylori has been identified as a definite carcinogen by the IARC, causing severe gastric diseases like peptic ulcer and gastric cancer. However, its role as the sole pathogen in gastric diseases is heavily debated, with factors like virulence proteins, geography and climate, host genetics and immunity, microbiota, and dietary habits playing a cumulative role in determining clinical outcomes.
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.
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