H. pylori and Human Gut Microbiota

Review Article

J Bacteriol Mycol. 2018; 5(8): 1086.

H. pylori and Human Gut Microbiota

Shiotani A¹*, Matsumoto H¹, Fukushima S¹, Katsumata R¹, Kawano M² and Saito M²

¹Department of Internal Medicine, Kawasaki Medical School, Japan

²Department of Microbiology, Kawasaki Medical School, Japan

*Corresponding author: Shiotani A, Department of Internal Medicine, Kawasaki Medical School, Private University in Kurashiki, Japan

Received: October 30, 2018; Accepted: November 26, 2018; Published: December 03, 2018

Abstract

The composition of the Gastrointestinal (GI) microbiome is shaped by a variety of factors including diet, additional environmental elements, and the genetic background of the host.

Recent evidence supports that H. pylori is the most relevant, but may not be the only local causative bacteria leading to gastric diseases. In several recent reports, a real, active cross talk between H. pylori and the other components of the gastric microbiota was observed. In this review, we provide a comprehensive review about gastric microbiota and discuss emerging concepts for the influence of H. pylori infection on gastric microbiome and vice versa.

H. pylori Infection and Gastric Microbiota

GI microbiota had been investigated by cultivation of luminal contents or mucosal biopsies, and the human stomach was long thought to be sterile. The new nucleotide sequencing techniques and advanced bioinformatics tools have opened the field for studying the diversity and complexity of the GI microbiome independent of traditional cultural methods. Increasing number of papers focus on non-H. pylori microbial community observed in the human stomach, so called human gastric microbiota [1]. Recent evidence supports that H. pylori is the most relevant, but may not be the only local causative bacteria leading to gastric diseases. The discrepancies of the results in the previous studies are likely due to different methods used for microbiota analysis, the limited sample sizes, difference in H. pylori infection rates, and several environmental factors such as diet, lifestyle, geography, and ethnicity. In several recent reports, a real, active cross talk between H. pylori and the other components of the gastric microbiota was observed. In this review, we provide a comprehensive review about gastric microbiota and discuss emerging concepts for the influence of H. pylori infection on gastric microbiome and vice versa.

Human stomach had been thought to be sterile, and following H. pylori discovery, it was thought to be the only bacterium able to colonize the gastric epithelium. Gastric environment is difficult to colonize mainly because of gastric acid barrier. Therefore, the microbial load is much less in the stomach than in the colon (1010- 1012 Colony-Forming Units (CFU)/mL) or been small intestine (102-104 CFU/mL) [2]. Gastric microbiota has previously identified by cultivation of gastric juice or mucosa biopsies. In the healthy stomach, the predominant bacteria belong to the species Clostridium, Lactobacillus and Veillonella based on culture analysis [3]. In the atrophic gastritis with the absence of H. pylori, urease producing members of the gastric microbiota, such as Proteus mirabilis, Klebsiella pneumonia, Staphylococcus aureus, Staphylococcus capitis, and Micrococcus species can cause false positive results in urea breath tests [4].

Recent advance of molecular biology, computer technology and bioinformatics allow genetic analysis of complex microbiota without cultivation, and the 16S rDNA sequence has opened a field for extensively revealing novel and uncultivated bacterial species in human stomach [5,6]. In the healthy stomach, the predominant bacteria belong to the phyla of Actinobacteria, Bacteroidetes, Firmicutes, and Proteobacteria (which include H. pylori), and genus of Streptococcus [7-9]. Utilizing a newer technology, tagged 454 pyrosequencing, analysis of H. pylori-negative biopsy samples identified 262 phylotypes representing 13 phyla [10]. The composition of the gastric microbiome in H. pylori-negative individuals is highly diverse. Common phylotypes present in H. pylori-uninfected subjects include Streptococcus, Prevotella, and Gemella [7]. These findings lend further support to the gastric microbiota being highly diverse, despite significant variability in the microbial composition between individuals [7,8].

In contrast, among H. pylori-positive subjects, the microbiota is much more uniform and H. pylori represents the most abundant phylotype. H. pylori DNA accounts for >90% of all sequence reads in H. pylori-positive subjects [7], so it greatly reduces the overall diversity of the gastric microbiota. The most abundant phyla in H. pylori-colonized stomachs are Proteobacteria, Firmicutes, and Actinobacteria [10,11]. H. pylori-infected adults are likely to have higher abundances of Spirochaetes, Acidobacteria and non- Helicobacter Proteobacteria and relatively lower abundance of Actinobacteria, Bacteroidetes, Firmicutes compared to H. pyloriuninfected adults [10]. A study performed by Hu et al. [12] identified the non-H. pylori bacterial flora in gastric biopsy specimens taken from H. pylori positive patients using matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDITOF MS). The major species were Streptococcus, Neisseria, Rothia, and Staphylococcus, which differed from previous reports of healthy volunteers. Klymiuk et al. [13] recently conducted a prospective, multicenter, clinical trial of 30 gastric biopsy samples including CagA-negative and CagA-positive H. pylori. In their study, the genera Actinomyces, Granulicatella, Veillonella, Fusobacterium, Neisseria, Helicobacter, Streptococcus, and Prevotella are significantly different between the H. pylori-positive and negative sample groups. However, there is no significant correlation of H. pylori phylogeographic population or carriage of the cag PAI with microbiota composition [13].

Interestingly, Khosravi et al. [14,15] isolated Streptoccus mitis (S. mitis) and Lactobucillus fermentum (L. fermentum) from human gastric tissue biopsies, and they have shown that metabolites released by co-culturing S. mitis and H. pylori induced H. pylori to transform into viable but non-culturable coccoidal form in vitro. Streptococci seem to survive and develop in an acidic gastric environment as an indigenous microbiota of the gastric mucosa, which may inhibit the colonization by H. pylori. In contrast, L. fermentum improved S. mitis survival via secreting diffusible factors [15].

Citation: Shiotani A, Matsumoto H, Fukushima S, Katsumata R, Kawano M and Saito M. H. pylori and Human Gut Microbiota. J Bacteriol Mycol. 2018; 5(8): 1086.