ArticleScientific reports2022
Lactate causes downregulation of Helicobacter pylori adhesin genes sabA and labA while dampening the production of proinflammatory cytokines.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Pathogenicity and virulence ofVirulence · 2025Review
- Development of a multi-epitope vaccine against Helicobacter pylori using a novel saRNA technology through an immunoinformatics approach.Scientific reports · 2025Article
- Dual role of lactate in human health and disease.Frontiers in physiology · 2025Review
- Dysregulated macrophage immunity inFrontiers in immunology · 2025Review
- Metabolic reprogramming inFrontiers in cellular and infection microbiology · 2025Review
- Novel RNA-methylase HNRNPC promotes gastric cancer tumorigenesis by triggering the lactate-induced ferroptosis resistance.Frontiers in immunology · 2025Article
- Glycan-mediated adhesion mechanisms in antibiotic-resistant bacteria.BBA advances · 2025Article
- Anti-inflammatory effects of extracellular vesicles and cell-free supernatant derived from Lactobacillus crispatus strain RIGLD-1 on Helicobacter pylori-induced inflammatory response in gastric epithelial cells in vitro.Folia microbiologica · 2024Article
- Lactate metabolism promotes in vivo fitness during Acinetobacter baumannii infection.FEMS microbiology letters · 2024Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Chronic inflammation induced by Helicobacter pylori is strongly associated with gastric cancer development, which is influenced by both bacterial virulence and host genetics. The sialic acid-binding adhesin SabA and the MUC5AC-binding adhesin LabA are important H. pylori virulence factors that facilitate adhesion of the bacterium, which is a crucial step in colonization. Lactate utilization has been reported to play a key role in the pathogenicity of different bacterial species. However, this is poorly understood in H. pylori. In this study, we investigated the effect of lactate on H. pylori adhesin gene expression and the regulation of host inflammatory cytokines. We show that the bacterial adhesins SabA and LabA were downregulated at the transcriptional level during incubation of H. pylori with lactate. Downregulation of sabA required the involvement of the two-component system ArsRS, while labA was regulated via the CheA/CheY system, indicating differences in the regulation of these genes in response to lactate. The levels of the proinflammatory cytokines TNF and IL-6 in H. pylori-stimulated macrophages were reduced when lactate was present. Interestingly, glucose did not prevent the secretion of these cytokines. Taken together, our data suggest that lactate affects H. pylori adhesin gene expression and the host response upon infection.
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