Gastrointestinal (GI) diseases have caused an increasing burden, with more than 80 million deaths worldwide. Diarrheal diseases and cirrhosis are among the top 10 death-causing gastroduodenal diseases in developing and middle- to low-income countries. On the other hand, in developed and high-income countries, GI malignancies are one of the death-causing diseases, of which colon, liver, and gastric cancers are the most prevalent. Several factors highly influence the development of these gastroduodenal diseases, including host genetic polymorphisms related to vulnerability and environmental factors associated with diets, lifestyle habits, and infection pathogens, especially Helicobacter pylori (H. pylori). H. pylori is believed to cause several gastroduodenal diseases, including chronic gastritis, peptic ulcer diseases, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. Although H. pylori infection is highly associated with gastroduodenal diseases, several studies have reported the prevalence of gastritis in the absence of H. pylori infection. Even in more severe conditions such as premalignant or gastric adenocarcinoma, a low abundance of H. pylori was reported.
Based on the description above, researchers from the Department of Internal Medicine, Faculty of Medicine, RSUD Dr. Soetomo, Universitas Airlangga succeeded in publishing the results of a literature study in one of the leading international journals, Gut Pathogens . In this study, researchers reviewed the role of the gastric microbiota in the development of gastroduodenal disease and showed that H. pylori is not the only causative agent for the development of gastroduodenal diseases.
The result of the study showed that gastric mucosal-associated microbes such as Enterococcus, Pseudomonas, Staphylococcus, and Stomatococcus were discovered in the early phase of molecular method studies. A study conducted in the United States that identified gastric microbial communities in patients with gastric disease found 128 kinds of phylotypes belonging to five major phyla of Proteobacteria, Firmicutes, Bacteroidetes, Actinobacteria, and Fusobacteria with 1506 types of non-H. pylori bacteria. These findings led to a new perspective on the gastric microbial environment as a whole system responsible for the pathogenesis of the disease.
A study conducted in Mongolia consisting of 11 patients with H. pylori-negative gastritis revealed a similar diversity index between these patients and individuals with normal mucosa. The relative abundance in the H. pylori-negative group showed a decreased amount Proteobacteria and increments in the Bacteroidetes population with the introduction of Spirochaetes as compared with the healthy group, in which the proportions of Proteobacteria, Bacteroidetes, and Firmicutes were evenly distributed. In indonesia, H.pylori-negative gastritis was observed in approximately 27% of all gastritis cases with increasing abundance of Paludibacter sp. These findings suggest that, even in the absence of H. pylori, it is still possible to detect typical gastritis caused by infection and altered gastric microbiota.
A study conducted in South Korea showed that the associated bacteria in the gastric cancer population were H. pylori, Propionibacterium acnes, and Prevotella copri. The overabundance of P. acnes is associated with enhancement of gastric cancer development via the production of proinflammatory cytokines such as IL-15. It has been strongly suggested that P. copri induces inflammatory conditions. In addition, recent findings showed an increased abundance of lactic acid bacteria (LAB): Streptococcus, Lactobacillus, Bifidobacterium, and Lactococcus also have role in gastric cancer development through several mechanisms, including the production of N-nitroso compounds, reactive oxygen species, and anti-H. pylori properties.
Based on this literature study, it can be conclude that the involvement of H. pylori in the development of gastroduodenal diseases is an indisputable factor. However, recent findings on gastric microbiota in some spectrum diseases showed remarkably smaller populations of H. pylori and increments of other bacteria in gastric carcinogenesis, suggesting that H. pylori may not be the only pathogen responsible for the pathogenesis of the disease.
Author: Muhammad Miftahussurur
Details of this study can be viewed on:
https://gutpathogens.biomedcentral.com/articles/10.1186/s13099-022-00494-0
