The State and Role of Esophagus, Stomach, Intestinal Microbiota in Patients With Ulcer Disease, Chronic Gastritis, Esophagitis

Abstract

The microflora of 64 biopsies taken during fibrogastroduodenoscopy of the mucous membrane of the esophagus, stomach and duodenum in healthy volunteers and 1120 samples obtained from the same parts of the digestive tract in patients with esophagitis, chronic gastritis and peptic ulcer disease were studied. The patients ranged in age from 18 to 62 years. Traditional bacteriological method was used to isolate and identify microorganisms. Staphylococcus spp., Streptococcus spp., Lactobacillus spp., Bacteroides spp., Stomatococcus spp., Enterobacteriaceae, Corynebacterium spp., Micrococcus spp., Neisseria spp., Veilonella spp. were isolated from biopsies of healthy respondents in an average amount from 3.2 to 4.68 lg CFU/g. H.pylori was found in 60% (5.66 lg CFU/g) in the esophagus, in 33.3% of cases (5.12 lg CFU/g) from the fundal part of the stomach, in 44.4% (5.25 lg CFU/g) from the antral part of the stomach, in 5.5% (4.2 lg CFU/g) in the duodenal mucosa. In samples obtained from the inflamed and eroded mucous membrane of the esophagus, stomach and duodenum, opportunistic bacteria of the genera Klebsiella, Enterobacter, Proteus, Pseudomonas, Peptococcus, Actinomyces, yeast fungi of the genus Candida etc. were detected in an amount exceeding 4 lg CFU/g. H. pylori isolated in 6.3-16.7% of patients (4.25-4.6 lg CFU/g) and did not dominate in relation to other microorganisms, and in most cases had a low frequency of its occurrence. In patients with the recurrence of peptic ulcer disease, exacerbation of chronic gastritis and esophagitis, dysbiosis was developed, characterized by an increase in the species and quantitative composition of opportunistic microflora, an increase in its enzymatic and cytotoxic activity, which can contribute to the maintenance of inflammatory and necrotic processes and inhibit the elimination of the pathological process.

Bile reflux alters the profile of the gastric mucosa microbiota

“…increase in inflamed and eroded mucous membranes of the esophagus, stomach, and duodenum. (Chervinets et al, 2020) Pseudomonas aeruginosa is also shown to promote gastric tumorigenesis in colonized rats. (Morishita and Shimizu, 1983) Increases in the abundance of this and other bacteria in patients with bile reflux may reflect a potential relationship between the bile reflux-specific microbiome and the occurrence and development of GC.…”

Integrating microbiome and metabolome revealed microbe-metabolism interactions in the stomach of patients with different severity of peptic ulcer disease

“…examined 128 phylotypes from human gastric biopsy samples, which were classified into five different bacterial phyla: Proteobacteria , Actinobacteria , Firmicutes , Fusobacteria , and Bacteroidetes ( 12 ). The diversity of microorganisms in the gastric environment was significantly different from that in the oral cavity, esophagus, and intestine ( 9 , 11 – 13 ). Although the mechanistic events involved in the development of PUD by Helicobacter pylori have been identified ( 6 ), the profile of the microbial community in the stomach at different pathological stages of PUD has not been systematically characterized.…”

“…The inflammatory process and severity of PUD may be related to structural changes in the gastric flora ( 10 ). Ecological dysbiosis of the gastric microbiota can induce a significant increase in the number and variety of opportunistic pathogenic bacteria, which can be toxic to cells and induce inflammation in the stomach ( 11 ). Bik et al.…”

“…However, most of the current research on gastrointestinal diseases has focused on the gut microbes and ignored the presence of specific gastric flora, and the potential mechanisms for the involvement of gastric flora are far from being explored in the development of PUD. The inflammatory process and severity of PUD may be related to structural changes in the gastric flora (10). Ecological dysbiosis of the gastric microbiota can induce a significant increase in the number and variety of opportunistic pathogenic bacteria, which can be toxic to cells and induce inflammation in the stomach (11).…”

Mikrobiota esophagus, stomach and duodenal estate in normal and pathology

“…Помимо H. pylori, микрофлора биоптатов желудка содержит бактерии 6 таксонов, включая: Proteabacteria, Firmicutes, Actinobacteria, Bacteroides, Fusobacteria и Deinococcus. Позитивная роль микробиоты связана с синтезом органических кислот, лизоцима, бактериоцинов и перекиси водорода, конкуренцией за источники питания и рецепторы адгезии, с усилением барьера, подавляющего транслокацию микробов из просвета кишечника во внутреннюю среду макроорганизма, нейтрализацией токсинов и токсических веществ [8]. Стимуляция иммунитета происходит за счет повышения параметров Т-и В-клеточного иммунитета, увеличения авидности антител сыворотки крови к связыванию антигенов патогенных микробов и их токсинов, регуляции синтеза 6-ти провоспалительных и 2-х противовоспалительных (IL-4 и IL-10) цитокинов.…”