The interruption of human gastric microbiota has been identiﬁed as a trigger of different diseases of the stomach.
It is observed in patients with atrophic gastritis that, less gastric acid barrier allows the occupation of the stomach by more microbes as compare to the healthy conditions with a physiologic acid secretion. However, limited data on gastric microbiota composition in patients with atrophic gastritis are presently accessible. Overall, microbial abundance was positively correlated with serum pepsinogen I/pepsinogen II ratio in Asian patients (Yu G et al., 2014).
Day by day it is becoming more evident that gastric microbiota is reason behind the development of gastrointestinal cancer. Microbes by different mechanisms can initiate and continue the growth of carcinogenic pathways, including the stimulation of inﬂammation, the increase in cell proliferation, the dyes- regulation of stem cell physiology, and the production of several metabolites (Abreu and Peek, 2014). Although H. pylori is the most related microbial issue for the expansion of gastric cancer, other components of the gastric microbiota are also involved in gastric carcinogenesis. The 16S rRNA gene sequencing analysis of gastric mucosa of patients with gastric cancer showed a occurrence of the genera Lactobacillus, Streptococcus (among which the most common species were S. mitis and Strep- tococcus parasanguinis), Prevotella, and Veillonella (Dicksved et al., 2009). Two studies evaluated the gastric microbiota of subjects with non-atrophic gastritis, intestinal metaplasia, and gastric cancer. In the ﬁrst type, the microbiota analysis was done with the microarray G3 PhyloChip, showing a signiﬁcantly lower variety and a higher copiousness of the genus Pseudomonas in the microbiota of neoplastic patients compared to patients with simple gastritis; furthermore, both the progressive decrease of six taxa (two species from TM7 phylum, two Porphyromonas sp, Neisseria sp, and Streptococcus sinensis) and the progressive increase of two taxa (Lactobacillus coleohominis and Lachnospiraceae) were observed from the gastritis group to the neoplastic group, via the metaplastic group (Aviles et al., 2014). In the second study, a high throughput sequencing platform (454 GS FLX Titanium) was used for the calculation of gastric microbiota in the three groups, showing totally diverse results: a more bacterial diversity, a comparative rise of Bacilli and Streptococcic, and a relative decrease of Helicobacteraceae were present in the cancer group related to other groups. The analysis of UniFrac distance between the three groups was done in both studies, getting similar results, that is, a clear parting between the neoplastic group and the gastritis group was found, as well as an connection of the metaplastic group with the two other groups (Eun et al., 2014).