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- Quorum Quenching Potential of Reyranella sp. Isolated from Riverside Soil and Description of Reyranella humidisoli sp. nov.
- Dong Hyeon Lee, Seung Bum Kim
- J. Microbiol. 2024;62(6):449-461. Published online May 30, 2024
- DOI: https://doi.org/10.1007/s12275-024-00131-2
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Abstract
- Quorum quenching refers to any mechanism that inhibits quorum sensing processes. In this study, quorum quenching activity among bacteria inhabiting riverside soil was screened, and a novel Gram-stain-negative, rod shaped bacterial strain designated MMS21-HV4-11(T), which showed the highest level of quorum quenching activity, was isolated and subjected to further analysis. Strain MMS21-HV4-11(T) could be assigned to the genus Reyranella of Alphaproteobacteria based on the 16S rRNA gene sequence, as the strain shared 98.74% sequence similarity with Reyranella aquatilis seoho-37(T), and then 97.87% and 97.80% sequence similarity with Reyranella soli KIS14-15(T) and Reyranella massiliensis 521(T), respectively. The decomposed N-acyl homoserine lactone was restored at high concentrations under acidic conditions, implying that lactonase and other enzyme(s) are responsible for quorum quenching. The genome analysis indicated that strain MMS21-HV4-11(T) had two candidate genes for lactonase and one for acylase, and expected protein structures were confirmed. In the quorum sensing inhibition assay using a plant pathogen Pectobacterium carotovorum KACC 14888, development of soft rot was significantly inhibited by strain MMS21-HV4-11(T). Besides, the swarming motility by Pseudomonas aeruginosa PA14 was significantly inhibited in the presence of strain MMS21-HV4-11(T). Since the isolate did not display direct antibacterial activity against either of these species, the inhibition was certainly due to quorum quenching activity. In an extended study with the type strains of all known species of Reyranella, all strains were capable of degrading N-acyl homoserine lactones (AHLs), thus showing quorum quenching potential at the genus level. This is the first study on the quorum quenching potential and enzymes responsible in Reyranella. In addition, MMS21-HV4-11(T) could be recognized as a new species through taxonomic characterization, for which the name Reyranella humidisoli sp. nov. is proposed (type strain = MMS21-HV4-11( T) = KCTC 82780( T) = LMG 32365(T)).
- Helicobacter pylori-mediated gastric pathogenesis is attenuated by treatment of 2-deoxyglucose and metformin
- Hanfu Su , Eun-Jung Bak , Aeryun Kim , Kavinda Tissera , Jeong-Heon Cha , Sungil Jang
- J. Microbiol. 2022;60(8):849-858. Published online June 22, 2022
- DOI: https://doi.org/10.1007/s12275-022-2130-z
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- 3 Citations
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Abstract
- Helicobacter pylori infection causes chronic inflammation in the stomach, which is linked to the development of gastric cancer. The anti-inflammatory and anticancer effects of a glycolysis inhibitor 2-deoxyglucose (2DG) and an antidiabetic medication metformin (Met) have gotten attention. Using a Mongolian gerbil animal model, we investigated H. pylorimediated gastric pathogenesis and how this pathogenesis is influenced by 2DG and Met. Five-week-old male gerbils were infected with H. pylori strain 7.13. After 2 weeks of infection, gerbils were fed 2DG-containing food (0.03% w/w), Met-containing water (0.5% w/v), or both (Combi) for 2 (short-term) or 10 weeks (long-term). Gastric pathogenesis and host response to H. pylori infection were examined by macroscopic and histopathologic analysis of gerbils’ stomach. As a result, indicators of gastric pathogenesis by H. pylori infection including infiltration of polymorphonuclear neutrophils and lymphocytes, intestinal metaplasia, atrophy, and proliferation of gastric epithelial cells were attenuated by short-term administration of 2DG, Met, or Combi. When the infection was sustained for long-term, gastric pathogenesis in drug-treated gerbils was equivalent to that in untreated gerbils, with the exception that the infiltration of neutrophil was reduced by 2DG. Colonization of H. pylori in stomach was unaffected by both short- and long-term treatments. Our findings demonstrate that the progression of gastric pathogenesis induced by H. pylori infection can be attenuated by the shortterm individual or combinational treatment of 2DG and Met, implying that 2DG or Met could be considered as a treatment option for gastric diseases in the early stages of infection.
- Function of Rhs proteins in porcine extraintestinal pathogenic Escherichia coli PCN033
- Wenjia Lu , Jia Tan , Hao Lu , Gaoyan Wang , Wenqi Dong , Chenchen Wang , Xiaodan Li , Chen Tan
- J. Microbiol. 2021;59(9):854-860. Published online August 12, 2021
- DOI: https://doi.org/10.1007/s12275-021-1189-2
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- 4 Citations
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Abstract
- Extraintestinal pathogenic Escherichia coli (ExPEC) is an important zoonotic pathogen that places severe burdens on public health and animal husbandry. There are many pathogenic factors in E. coli. The type VI secretion system (T6SS) is a nano-microbial weapon that can assemble quickly and inject toxic effectors into recipient cells when danger is encountered. T6SSs are encoded in the genomes of approximately 25% of sequenced Gram-negative bacteria. When these bacteria come into contact with eukaryotic cells or prokaryotic microbes, the T6SS assembles and secretes associated effectors. In the porcine ExPEC strain PCN033, we identified four classic rearrangement hotspot (Rhs) genes. We determined the functions of the four Rhs proteins through mutant construction and protein expression. Animal infection experiments showed that the Δrhs-1CT, Δrhs-2CT, Δrhs-3CT, and Δrhs-4CT caused a significant decrease in the multiplication ability of PCN033 in vivo. Cell infection experiments showed that the Rhs protein is involved in anti-phagocytosis activities and bacterial adhesion and invasion abilities. The results of this study demonstrated that rhs1, rhs3, and rh4 plays an important role in the interaction between PCN033 and host cell. Rhs2 has contribution to cell and mice infection. This study helps to elucidate the pathogenic mechanism governing PCN033 and may help to establish a foundation for further research seeking to identify potential T6SS effectors.
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