At general level, the gastric microbiota composition is quite dynamic, so affected by variety of factors, like medication use, dietry habits as well as swelling of gastric mucosa and colonization of H. pylori also. Studies reveal the effect of dite in human gut microbiota composition, but there are very little evidences that are mainly restricted to animal model research studies.
The long-term use of proton pump inhibitors (PPIs) and H2-antagonists, as well as atrophic gastritis, aﬀects the composition of the gastric microbiota; this is not surprising, considering that gastric microbiota depends on gastric acid secretion. Bacterial overgrowth occurs when the gastric pH was >3.8. Antibiotics are known to have negative ecological eﬀects on gastrointestinal microﬂora. Animal studies show that penicillin treatment reduces Lactobacilli populations and promotes yeast colonization of the gastric epithelium. Using culture-dependent and cul- ture-independent approaches, Mason et al.26 demonstrated that cefoperazone treatment in the human causes long-term alteration of gastric microbiota, such as a signiﬁcant reduction in the number of Lactobacilli and overgrowth of Enterococci.
Relationship between Helicobacter pylori and gastric microbiota:
Studies in animal models show that long-term H. pylori infection aﬀects the bacterial composition of the gastric microbiota. Indeed, an abundance of Eubacterium cylindroides and Prevotella species and a decrease of Biﬁdobacterium species, Clostridium coccoides and Clostridium leptum were found in H. pylori-negative, but not in H. pylori-positive gerbils. Studies con- ducted in patients without H. pylori infection reveal that they have a relative lack of Proteobacteria and Bacteroidetes phyla, and a relative abundance of Streptococcus and Prevotella genera. In H. pylori- positive patients, with respect to H. pylori-negative sub- jects, Maldonado-Contreras et al.28 report a higher abundance of Proteobacteria, Spirochetes and Acidobacteria; and a decreased abundance of Actinobacteria, Bacteroidetes and Firmicutes. H. pylori-induced changes in gastric microﬂora can be attributed to various factors. Long-term H. pyloriInfection leads to gastric atrophy, and consequently, to an increase of the gastric pH, which prompts the colonization of the stomach by transient bacteria. In addition, ammonia and bicarbonate produced by H. pylori from urea may serve as substrates for other bacteria. Finally, H. pylori slows gastric motility, thereby favoring the clearance of adherent bacteria from the mucosa. It is likely that H. pylori creates special niches that allow the survival and colonization of bacteria in the stomach. Notwithstanding these ﬁnd- ings, the relationship between H. pylori and the gastric microbiota is still controversial. Indeed, Tan et al.29 report that chronic H. pylori infection does not signiﬁ- cantly alter the microbiota of the murine stomach. Similarly, Bik et al. did not ﬁnd signiﬁcant diﬀerences in gastric microbiota between H. pylori-positive and H. pylori-negative patients, in terms of 16S rDNA sequences. Very recently, Khosravi et al.30 conﬁrmed these ﬁndings in a large sample of subjects, including 131 H. pylori-positive and 84 H. pylori-negative patients. It is likely that factors such as the degree of H. pylori-related inﬂammation; the time of the infec- tion; and the presence, type and extension of precan- cerous lesions have to be taken into account, when dealing with the composition of gastric microbiota. (G. Nardone and D. Compare, 2014)
Different colonies of Gut microbiota are present in stomach and also in whole gastrointestinal tract. However, because of low pH in gastric environment it is very difﬁcult to colonize, there is median pH 1.4 in that area.That’s why, the number of microbes is lesser in stomach as compare to in the colon or the small intestine. (102– 104 colony-forming units (CFU)/mL of bacteria in thestomach compared to 1010–1012 CFU/mL in the colon) (Marshall and Warren, 1984).
At initial, by using conventional methods the presence of microorganisms was reported in human stomach other than H. pylori, including the histologic analysis of gastric specimens and the culture of gastric juice and gastric mucosa. After culture analysis, it is obvious that under healthy conditionsClostridium sp, Lactobacillus sp and Villanelle sp were the most representative bacteria of the human stomach (Delgado et al., 2011). However, almost 80% of microbes are not able to cultivate and that’s why in order to get reliable information only the application of culture-independent, molecular approaches (e.g., gene sequencing) for the analysis of gastric microbiota can be used. Under healthy conditions, the main bacteria belong to the phyla of Actinobacteria, Bac- teroidetes, Firmicutes, and Proteobacteria (which include H. pylori); the predominant genus is Streptococcus. More recently, it was revealed that the microbiota of the stomach has totally different composition as compare to microbiota of the mouth or throat; accordingly, gastric microbiota appears to be comprised of occupant microbes rather than microorganisms of upper organs. As Western reports reveals that the gastric microbiota of H. pylori -negative subjects has a higher diversity than that of H. pylori -positive patients (Andersson et al., 2008). Two L. reuteri strains, separated from gastric juice and biopsies, showed a high antimicrobial result against H. pylori, collectively have good confrontation to the acidic atmosphere of the stomach (Delgado et al., 2015). Also, a commensal microorganism of the human stomach Streptococcus mitis, had the ability to stop the growth of H. pylori(using a metabolomic analysis method) and convert it from spiral to a coccoidal type (Khosravi et al ., 2014).