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Sphingomonas ginsenosidimutans sp. nov., with Ginsenoside Converting Activity
최태은,Qing-Mei Liu,Jung-Eun Yang,Siyi Sun,김세영,이태후,임완택 한국미생물학회 2010 The journal of microbiology Vol.48 No.6
The Gram-reaction-negative, strictly aerobic, non-motile, non-spore-forming, and rod-shaped bacterial strain designated Gsoil 1429T was isolated from the soil of ginseng cultivating field of Pocheon province in South Korea. This bacterium was characterized in order to determine its taxonomic position by using the polyphasic approach. Strain Gsoil 1429T grew well at 25-37°C and at pH 7.0 on R2A and nutrient agar without NaCl supplement. Strain Gsoil 1429T had β-glucosidase activity, which was responsible for its ability to transform ginsenoside Rb1 (one of the dominant active components of ginseng) to F2 via gypenoside XVII. On the basis of 16S rRNA gene sequence similarity, strain Gsoil 1429T was shown to belong to the family Sphingomonadaceae and to be related to Sphingomonas yunnanensis YIM 003T (98.2% sequence similarity), S. phyllosphaerae FA2T (97.5%), S. koreensis JSS26T (97.3%), and S. asaccharolytica IFO 15499T (97.1%). The G+C content of the genomic DNA was 65.6%. The major respiratory quinone was Q-10 and the major fatty acids were summed feature 8 (comprising C18:1 ω7c/ω9t/ω12t), C16:0 and C14:0 2OH. DNA and chemotaxonomic data supported the affiliation of strain Gsoil 1429T to the genus Sphingomonas. The DNA-DNA relatedness values between strain Gsoil 1429T and its closest phylogenetically neighbours were below 28%. Strain Gsoil 1429T could be differentiated genotypically and phenotypically from the recognized species of the genus Sphingomonas. The isolate therefore represents a novel species, for which the name Sphingomonas ginsenosidimutans sp. nov. is proposed, with the type strain Gsoil 1429T (=KACC 14949T =JCM 17074T =LMG 25799T).
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Metabolism Characteristics of Mycoplasma pneumoniae Infection in Asthmatic Children
Luo Jiaying,Chen Huian,Zhang Qiyong,Huang Xinyun,Qin Xu,Li Jing,Chen Siyi,Xiao Yongxin,Sun Lihong,Sun Baoqing 대한천식알레르기학회 2022 Allergy, Asthma & Immunology Research Vol.14 No.6
Purpose: Studies have shown that Mycoplasma pneumoniae (Mp) infection can aggravate symptoms in asthmatics. However, the mechanism by which Mp infection exacerbates asthma remains unclear. Metabolomics can help identify the mechanism of Mp aggravating asthma in children, thereby providing more a potential target for improving clinical treatment programs. In this article, we analyzed the metabolic level of patients to explain how Mp aggravates asthma in children. Methods: We divided the subjects into the asthma, Mp infection, asthma combined with Mp infection and healthy groups. Patients’ peripheral blood was collected for metabolic and interaction analysis. Cytokine levels were measured via serum and exhaled breath condensate (EBC). Results: A total of 150 participating subjects were divided into four groups after exclusion. We found out that there were different metabolic pathways between the healthy and disease groups. The major pathways of both asthma and asthma combined with Mp infection were valine, leucine and isoleucine biosynthesis; malate-aspartate shuttle was the main differential pathway for Mp infection. Moreover, even though three disease groups involved 81 metabolites at the same time, compared with asthma combined with Mp infection, 2 single disease groups still involved different amino acid pathways (phenylalanine, tyrosine and tryptophan biosynthesis; valine, leucine and isoleucine biosynthesis). Interaction analysis showed that Mp infection in asthmatic patients not only activated cytokines, but also activated Toll-like receptors (TLRs) 2 and 6. Finally, the levels of interleukin (IL)-4, IL-8, IL-13 and tumor necrosis factor-α in EBC with asthma combined with Mp infection were significantly higher than the 2 single disease groups. Conclusions: Mp infection in asthmatic children can cause changes in the levels of various amino acids in the body, which were enriched in the pathways such as valine, leucine and isoleucine biosynthesis. Palmitic acid can activate TLR2, and iloprost reduces IL-10 levels, ultimately leading to the increased airway inflammation.
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