Abstract
Helicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the stomach and can induce gastric disease and intra-gastric lesions, including chronic gastritis, peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. This bacterium is responsible for long-term complications of gastric disease. The conjunction of host genetics, immune response, bacterial virulence expression, diet, micronutrient availability, and microbiome structure influence the disease outcomes related to chronic H. pylori infection. In this regard, the consumption of unhealthy and unbalanced diets can induce microbial dysbiosis, which infection with H. pylori may contribute to. However, to date, clinical trials have reported controversial results and current knowledge in this field is inconclusive. Here, we review preclinical studies concerning the changes produced in the microbiota that may be related to H. pylori infection, as well as the involvement of diet. We summarize and discuss the last approaches based on the modulation of the microbiota to improve the negative impact of H. pylori infection and their potential translation from bench to bedside.
Highlights
Helicobacter pylori, considered the main bacterium responsible for gastric disease and long-term complications [1], is a Gram-negative bacterium that colonizes the stomach [2]
vacuolating cytotoxin (VacA) accumulation in different host cell compartments can have many consequences related to gastric inflammation and, gastric carcinogenesis, such as the induction of apoptosis [8] and autophagic cell death [9], the disruption of gastric epithelial cell tight junctions [10], the suppression of host T cell proliferation and activation by yet to be discovered mechanisms [11], and the modulation of host cell metabolism [12]
H. pylori infection is the major cause of the development of gastric and duodenal ulcers and gastric cancer worldwide, affecting almost 50% of the world’s population
Summary
Helicobacter pylori, considered the main bacterium responsible for gastric disease and long-term complications [1], is a Gram-negative bacterium that colonizes the stomach [2]. In the strains that carry the CagA gene, the CagA protein enters the host gastric cells upon H. pylori secretion, where it is phosphorylated and causes changes in cell morphology that lead to disturbed cell function by affecting multiple signaling pathways. H. pylori infection impairs the gastric tissue microenvironment, and promotes epithelial-mesenchymal transition and further gastric cancer progression [17]. In this line, dietary habits such as a high intake of green tea, fruits, or vegetables showed benefits against gastric cancer risk. In the context of chronic H. pylori infection, the intersection of host genetics, immune response, bacterial virulence expression, diet, micronutrient availability, and microbiome structure influence disease outcomes [18] (Figure 1). Adenlismaarel arnodutiinnevliytruosmedodtoeltsesatrethreoueftfiincealcyyuosfeedmerging treatmtoentetsstftohrethefefiecraacdyicoaftieomneorfgHin.gptyrleoarit.mTehnetssefaopr pthroeaecrhaedsicmataiionnlyoffoHcu. spyolnortih. eThinehseibaitpiopnrooarchreevsemrsaailnolyf afdocvuesrsoeneftfheectisnbhyibaitvioonidoinrgrethveerastatlaochf madevnetrasnedefcfoelcotsnibzyataiovnoiodfinhgostthientestinal epithevaltiitaaatlciochenmlsls:eLnatPnadSn,tldhipecooapltotoenlnyiuzsaaatctiicoohnnaooriffdtheho,esTtcLoiRnnt4see,sqttouinlela-nllickeeepsirotehfcetehlpieatlohcroes4ltl,sasanpndrdoT-tNihneFfl-aaαtmt,etmnuuamtaootriroynnsetocafrtoethsaiesftcefoarcnHtso.erpq-yaulleopnrhicaien.sfeocfttiohne.hAobstbrsepvriaot-iionnflsa: mLPmSa, tloipryopsotalytesaacfctherarHid. ep,yTloLrRi i4n,fteocltli-olink.eArebcberpet-or 4, and TNF-α, tumor necrosis factor-alpha
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