Role of Helicobacter pylori and Other Environmental Factors in the Development of Gastric Dysbiosis

Abstract

Microbiomes are defined as complex microbial communities, which are mainly composed of bacteria, fungi, and viruses residing in diverse regions of the human body. The human stomach consists of a unique and heterogeneous habitat of microbial communities owing to its anatomical and functional characteristics, that allow the optimal growth of characteristic bacteria in this environment. Gastric dysbiosis, which is defined as compositional and functional alterations of the gastric microbiota, can be induced by multiple environmental factors, such as age, diet, multiple antibiotic therapies, proton pump inhibitor abuse, H. pylori status, among others. Although H. pylori colonization has been reported across the world, chronic H. pylori infection may lead to serious consequences; therefore, the infection must be treated. Multiple antibiotic therapy improvements are not always successful because of the lack of adherence to the prescribed antibiotic treatment. However, the abuse of eradication treatments can generate gastric dysbiotic states. Dysbiosis of the gastric microenvironment induces microbial resilience, due to the loss of relevant commensal bacteria and simultaneous colonization by other pathobiont bacteria, which can generate metabolic and physiological changes or even initiate and develop other gastric disorders by non-H. pylori bacteria. This systematic review opens a discussion on the effects of multiple environmental factors on gastric microbial communities.

Lactobacillus rhamnosus GG supplementation on eradication rate and dyspepsia in Helicobacter pylori infection treated with three-in-one bismuth quadruple therapy

“…By itself, patients with functional dyspepsia have alterations in the gastric microbiota and, in some cases, treatment with probiotics resulted in the improvement of functional dyspepsia ( Nakae et al, 2016 ; Ohtsu et al, 2017 ; Wauters et al, 2020 ). Furthermore, the presence of Hp in the stomach causes the development of different environments for bacterial growth ( Hunt et al, 2015 ) that results more relevant than the alterations induced by hypochlorhydria alone ( Parsons et al, 2017 ; Gomez-Ramirez et al, 2021 ). The subversion of the gastric microbiota due to Hp infection may be related to the intrinsic properties of the bacterium that can create a hostile environment, making it difficult for the other bacteria to survive, thus allowing the establishment of a condition of gastroduodenal dysbiosis ( Bruno et al, 2018 ; Gomez-Ramirez et al, 2021 ).…”

“…Furthermore, the presence of Hp in the stomach causes the development of different environments for bacterial growth (Hunt et al, 2015) that results more relevant than the alterations induced by hypochlorhydria alone (Parsons et al, 2017;Gomez-Ramirez et al, 2021). The subversion of the gastric 10.3389/fmicb.2022.932331 microbiota due to Hp infection may be related to the intrinsic properties of the bacterium that can create a hostile environment, making it difficult for the other bacteria to survive, thus allowing the establishment of a condition of gastroduodenal dysbiosis (Bruno et al, 2018;Gomez-Ramirez et al, 2021). In Hp-positive subjects, molecular analyses showed a reduction in biodiversity with the absolute prevalence of Hp, followed by Streptococcus (Klymiuk et al, 2017).…”

“…The efficacy of eradication treatment on the improvement of dyspepsia, which is associated with the type of antibiotic used, also suggests a possible role of dysbiosis in the onset and persistence of dyspepsia after Hp eradication ( Kim et al, 2017 ). Indeed, Hp infection could create a microenvironment that facilitates the proliferation of some bacterial species, despite beneficial ones, that often perpetuates after the infection eradication, partially due to irreversible mucosal alterations caused by Hp infection, and that creates a new gastric microenvironment favored by host-related factors ( Gomez-Ramirez et al, 2021 ).…”

Assessing Helicobacter pylori motility and biofilm formation in subinhibitory concentrations of antimicrobials

“…Currently, this bacterium is considered a public health concern because it is classified as class I carcinogen and is associated with gastric adenocarcinoma and non-Hodgkin lymphoma development (STERBENC et al, 2019). Infection by H. pylori and disease progression are closely associated with host factors and H. pylori pathogenicity due to expression of virulence factors like flagella, heat shock proteins, urease, superoxide dismutase, and catalase, among others, which are essential for bacterial colonization, invasion, and survival in the gastric mucosa (BAJ et al, 2021;GOMEZ-RAMIREZ et al, 2021;STERBENC et al, 2019).…”

“…In the gastric mucosa, H. pylori develops swimming motility and moves through an attractive chemical gradient containing amino acids, mucin, urea, and sodium bicarbonate until it establishes close contact with epithelial cells; adhesion occurs through adhesin BabA (bound to the Lewis-b blood group) and outer membrane proteins (OMPs) SabA, HopZ, AlpA, AlpB, and OipA, which facilitates mucosa colonization and biofilm formation (ABDOLLAHI and TADJROBEHKAR, 2012;GU, 2017;HATHROUBI et al, 2018;CHMIELA and KUPCINSKAS, 2019;STERBENC et al, 2019;GOMEZ-RAMIREZ et al, 2021). Proteins LuxS and autoinducer 2 (AI-2) are also essential for maintaining the bacterium in the gastric epithelium and influence bacterial motility and biofilm formation (COLE et al, 2004;RADER et al, 2011;WANG et al, 2019).…”