ArticlePloS one2014
Identification of the genes that contribute to lactate utilization in Helicobacter pylori.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Added sugars, gut microbiota, and host health.Gut microbes · 2025Review
- Metabolic reprogramming inFrontiers in cellular and infection microbiology · 2025Review
- Study ofCancers · 2023Article
- Helicobacter pylori initiates successful gastric colonization by utilizing L-lactate to promote complement resistance.Nature communications · 2023Article
- Oral microbiota and Helicobacter pylori in gastric carcinogenesis: what do we know and where next?BMC microbiology · 2021Review
- Shedding Light on the African Enigma: In Vitro Testing ofMicroorganisms · 2021Article
- Gastric Metabolomics Detects Helicobacter pylori Correlated Loss of Numerous Metabolites in Both the Corpus and Antrum.Infection and immunity · 2021Article
- Article
- Comparative genomics analysis to differentiate metabolic and virulence gene potential in gastric versus enterohepatic Helicobacter species.BMC genomics · 2018Article
- Helicobacter pylori chemoreceptor TlpC mediates chemotaxis to lactate.Scientific reports · 2017Article
- Elucidation of the Metabolic Network of Helicobacter pylori J99 and Malaysian Clinical Strains by Phenotype Microarray.Helicobacter · 2017Article
- Epithelial Coculture and l-Lactate Promote Growth of Helicobacter cinaedi under H2-Free Aerobic Conditions.Applied and environmental microbiology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Helicobacter pylori are Gram-negative, spiral-shaped microaerophilic bacteria etiologically related to gastric cancer. Lactate utilization has been implicated although no corresponding genes have been identified in the H. pylori genome. Here, we report that gene products of hp0137-0139 (lldEFG), hp0140-0141 (lctP), and hp1222 (dld) contribute to D- and L-lactate utilization in H. pylori. The three-gene unit hp0137-0139 in H. pylori 26695 encodes L-lactate dehydrogenase (LDH) that catalyzes the conversion of lactate to pyruvate in an NAD-dependent manner. Isogenic mutants of these genes were unable to grow on L-lactate-dependent medium. The hp1222 gene product functions as an NAD-independent D-LDH and also contributes to the oxidation of L-lactate; the isogenic mutant of this gene failed to grow on D-lactate-dependent medium. The parallel genes hp0140-0141 encode two nearly identical lactate permeases (LctP) that promote uptake of both D- and L-lactate. Interestingly an alternate route must also exist for lactate transport as the knockout of genes did not completely prevent growth on D- or L-lactate. Gene expression levels of hp0137-0139 and hp1222 were not enhanced by lactate as the carbon source. Expression of hp0140-0141 was slightly suppressed in the presence of L-lactate but not D-lactate. This study identified the genes contributing to the lactate utilization and demonstrated the ability of H. pylori to utilize both D- and L-lactate.
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Registered trials
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