Helicobacter pylori-Induced Inflammation: Possible Factors Modulating the Risk of Gastric Cancer

• Published in: Pathogens (Basel) Vol. 10; no. 9; p. 1099
• Main Authors: Kumar, Sushil, Patel, Girijesh Kumar, Ghoshal, Uday C.
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 29-08-2021; MDPI
• Subjects: Cancer; Carcinogenesis; Carcinogens; Cell division; chronic inflammation; Cytokines; Digestive system; Disease; Exosomes; Gastric cancer; gastric carcinogenesis; Gastritis; Gastrointestinal tract; Gene polymorphism; Genetic factors; gut microbiota; Helicobacter pylori; Infections; Inflammation; intestinal helminth; Intestinal microflora; Intestine; Lesions; Medical prognosis; Microbiota; Review; Risk; Ulcers; Virulence
• ISSN: 2076-0817; 2076-0817
• DOI: 10.3390/pathogens10091099

Chronic inflammation and long-term tissue injury are related to many malignancies, including gastric cancer (GC). Helicobacter pylori (H. pylori), classified as a class I carcinogen, induces chronic superficial gastritis followed by gastric carcinogenesis. Despite a high prevalence of H. pylori infection, only about 1–3% of people infected with this bacterium develop GC worldwide. Furthermore, the development of chronic gastritis in some, but not all, H. pylori-infected subjects remains unexplained. These conflicting findings indicate that clinical outcomes of aggressive inflammation (atrophic gastritis) to gastric carcinogenesis are influenced by several other factors (in addition to H. pylori infection), such as gut microbiota, co-existence of intestinal helminths, dietary habits, and host genetic factors. This review has five goals: (1) to assess our current understanding of the process of H. pylori-triggered inflammation and gastric precursor lesions; (2) to present a hypothesis on risk modulation by the gut microbiota and infestation with intestinal helminths; (3) to identify the dietary behavior of the people at risk of GC; (4) to check the inflammation-related genetic polymorphisms and role of exosomes together with other factors as initiators of precancerous lesions and gastric carcinoma; and (5) finally, to conclude and suggest a new direction for future research.