The Relationship between H. Pylori Infection and Mitochondrial Microsatellite Instability in Gastric Carcinogenesis
Recent research has established that while there are a number of steps that take place in the development of gastric cancer, Helicobacter pylori (H. pylori) plays a major role. However, the mechanism of the influence remains unidentified. Researchers Ling et al. (2016) conducted a study to determine relationships between an infection of H. pylori, IL-8, and mtMSI and whether there is a trigger that causes the infection to progress to intestinal metaplasia, dysplasia, and ultimately to gastric carcinogenesis.
The method used by the researchers included fresh samples from resected gastric cancerous cells and comparison samples of potentially pre-cancerous mucosa; mucosa from patients with no diagnosed gastric disease was also gathered as a control. DNA genomes were identified. Participants were excluded who had a family history of colon cancer, had received chemotherapy or radiation therapy, or had received antibiotics or proton pump inhibitors in the last three months. Presence of the H. pylori infection was evaluated by histology testing and administration of a urease breath test. If one of the tests were positive, the participant qualified for inclusion in the study.
The results of the study found that in patients without H. pylori in normal gastric mucoa had significantly lower incidences of chronic gastritis, gastric cancer, dysplasia, and intestinal metaplasia; the rates of infection were within the range of 42.6 percent and 55 percent for infection. It was also found that a possible correlation between H. pylori infection and expressions of IL-8 and mtMSI exists, strongly influencing the development of gastric cancer. The suggestion is that early creation and accumulation of mtMSI in the cells of the gastric system as the same time as a H. pylori infection occurs is a crucial step in the pathway leading. It has been seen that an infection of H. pylori bacteria may cause mutations in mtDNA seen early in gastric carcinoma. For this reason, Ling et al. (2016) evaluated gastric mucosa that was either H. pylori-positive or H. pylori-negative with microsatellite markers changed in the presence of gastric cancer. It was found that as the cancer grows, mtMSI numbers increase and are significantly higher in mucosa that tested H. pylori-positive rather than H. pylori-negative. The mechanism by which this process occurs is unknown at the present time.
The conclusion of the study by Ling et al. (2016) is that mtMSI is a crucial event in the pathway that leads to the development of gastric carcinogenesis and the process is aided by an H. pylori infection. IL-8 may react with mtMSI altered by the bacteria in the infection. Therefore, the presence of mtMSI with an H. pylori infection may serve as a marker for potential development of gastric cancer. In addition, high levels of IL-8 may be indicative of more aggressive gastric carcinoma. Further study is required to determine the mechanisms of the interactions in order for them to serve as precursors of gastric carcinogensis. It is possible that treatment of H. pylori infections with antibiotics may reduce the incidence of gastric cancer. If patients suffering from ulcers or other gastric diseases display the presence of H. pylori bacteria, antibiotic therapy may be indicated. Again, further research is needed before this becomes an acceptable method of gastric cancer prevention.
References
Ling, X., Zhang, H., Shen, C., Yan, W., Wang, P., & Feng, J. et al. (2016). H. pylori infection is related to mitochondrial microsatellite instability in gastric carcinogenesis. Infectious Agents and Cancer, 11(1). http://dx.doi.org/10.1186/s13027-016-0078-5
