Association of Helicobacter pylori Infection and Host Cytokine Gene Polymorphism with Gastric Cancer

Abstract

The global cancer burden of new cases of various types rose with millions of death in 2018. Based on the data extracted by GLOBOCAN 2018, gastric cancer (GC) is the third leading cause of mortality related to cancer across the globe. Carcinogenic or oncogenic infections associated with Helicobacter pylori (Hp) are regarded as one of the essential risk factors for GC development. It contributes to the increased production of cytokines that cause inflammation prior to their growth in the host cells. Hp infections and specific types of polymorphisms within the host cells encoding cytokines are significant contributors to the hostʼs increased susceptibility in terms of the development of GC. Against the backdrop of such an observation is that only a small portion of the cells infected can become malignant. The diversities are a consequence of the differences in the pathogenic pathway of the Hp, susceptibility of the host, environmental conditions, and interplay between these factors. It is evident that hosts carrying cytokine genes with high inflammatory levels and polymorphism tend to exhibit an increased risk of development of GC, with special emphasis being placed on the host cytokines gene polymorphisms.

Blood index panel for gastric cancer detection

“…Studies have shown that the level of PG I can reflect the secretory function of gastric glands to a certain extent, and its level is positively correlated with the maximum secretion of gastric acid but negatively correlated with the degree of gastric body inflammation and atrophy[ 17 ]. An increase in the level of PG II suggests an inflammatory response in the gastric mucosa, while a decrease in the level of PG I suggests atrophy of the gastric corpus[ 13 ]. When the gastric mucosa atrophies and develops severe injury, the number of gastric glands and fundic glands will decrease or be replaced by pyloric glands, and the pyloric glands lack gastric chief cells and cervical mucous cells, which will lead to a decreases in the level of PG I and the ratio of PG I/II[ 18 ].…”

“…Cytokines produced by tumor cells or the tumor stroma can stimulate the survival, proliferation, and metastasis of cancer cells. These factors were demonstrated to be potential biomarkers for various cancers[ 13 - 15 ].…”

Helicobacter pylori-Associated Iron Deficiency Anemia in Childhood and Adolescence-Pathogenesis and Clinical Management Strategy

“…With regard to the initial stage of the colonization of H. pylori in the stomach, OMPs expressed on the bacterial surface are important as virulence factors and can bind to gastric epithelial cells [59]. The H. pylori genome has nearly 60 genes encoding the OMPs [60].…”

“…Toll-like receptors (TLRs) belong to the large family of pattern recognition receptors (PRRs) and are important in the innate immunity of the host [90]. Among the 10 types of TLRs identified in humans [91], TLR2 and TLR4 on the gastric epithelial and immune cells are both associated with recognition of LPS composing the cell wall of H. pylori, acting as a primary defense against H. pylori [60,92]. However, it seems that TLRs, including these two molecules can play opposite roles, either promotion or suppression of H. pylori infection as innate immunity [90].…”

“…Host genetic factors that affect cytokines may determine differences in the susceptibility or risk of infected individuals to specific H. pylori-associated diseases [70]. It is reported that various single-nucleotide polymorphisms (SNPs) of cytokines genes, such as tumor necrosis factor (TNF)-α, IL-1β, and IL-10, are associated with the risk of precancerous gastric pathology, including atrophic gastritis and intestinal metaplasia [60], although such an association remains controversial [70]. The allelic distribution of IL-1β is one of the most popular candidate gene studied on H. pylori infection [59].…”