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자연발효 과정에서 인디고에 환원력을 지닌 미생물 커뮤니티 분석과 농화배양
최은실(Eun-Sil Choi),이은빈(Eun-Bin Lee),최형안(Hyueong-An Choi),손경희(Kyunghee Son),김근중(Geun-Joong Kim),신윤숙(Younsook Shin) 한국생물공학회 2013 KSBB Journal Vol.28 No.5
Indigo is utilized in various industries including textile dyeing, cosmetics, printing and medicinal products and its reduced form, leuco-indigo, is mainly used in these process. Chemical reducing agent (sodium dithionite, sodium sulfide, etc.) is preferred to use for the formation of leucoindigo in industry. In traditional indigo fermentation process, microorganisms can participate in the reduction of indigo and thus it has been known to reduce environmental pollution and noxious byproducts. However, in fermentation method using microorganisms it is difficult to standardize large scale production process due to low yield and reproducibility. In this study, we attempted to develop the indigo reduction process using microbial flora which was isolated from naturally fermented indigo vat or deduced by metagenomic approach. From the results of library analyses of PCR-amplified 16S rRNA genes from the traditional indigo fermentation vat sample (metagenome), it was confirmed that Alkalibacteriums (71%) was distinctly dominant in population. Some strains were identified after confirming that they become pure culture in nutrient media modified slightly. Four strains were separated in this process and each strain showed obvious reducing ability toward indigo in dyeing test. It is expected that the analyzed results will provide important data for standardizing the natural fermentation of indigo and investigating the mechanism of indigo reduction.
Interleukin-13으로 유도된 폐 병태생리에 대한 atorvastatin의 치료 효과
모요셉 ( Yosep Mo ),배보람 ( Boram Bae ),김정현 ( Junghyun Kim ),김율담 ( Ruth Lee Kim ),손경희 ( Kyunghee Son ),강민종 ( Min-jong Kang ),이춘근 ( Chun-gen Lee ),조상헌 ( Sang-heon Cho ),강혜련 ( Hye-ryun Kang ) 대한천식알레르기학회(구 대한알레르기학회) 2021 Allergy Asthma & Respiratory Disease Vol.9 No.2
Purpose: Asthma is a common chronic lung disease, in which interleukin (IL)-13 is implicated as a central regulator of IgE synthesis, mucus hypersecretion, airway hyperresponsiveness (AHR), and fibrosis. This study was designed to determine the anti-inflammatory effect of atorvastatin, a widely used lipid-lowering agent, on the IL-13-induced lung pathology through the modulation of macrophages. Methods: Atorvastatin (40 mg/kg) was given to transgenic mice overexpressing IL-13 (IL-13 TG mice) and their wild type littermates by oral gavage for 2 weeks. AHR, numbers of inflammatory cells in the airway, and cytokine levels in IL-13 TG mice were measured. Using the alveolar macrophage cell line CRL-2456, the direct effect of atorvastatin on macrophages activated by recombinant IL-13 was assessed. Results: Significant reduction in total leukocytes and alleviation of AHR were observed with administration of atorvastatin in IL-13 TG mice compared to those without atorvastatin treatment (P<0.05). Atorvastatin administration resulted in upregulation of IL-10 in the lungs of IL-13 TG mice (P<0.05). In addition, mRNA expression of connective tissue growth factor, fibronectin, and type III collagen as well as chord length enhanced by IL-13 overexpression were reduced by atorvastatin administration (P<0.05). M2 macrophage markers, such as Ym-1 and CD206, were decreased, while M1 macrophage marker, inducible nitric oxide synthase, was increased upon atorvastatin treatment (P<0.05). Administration of atorvastatin resulted in improved removal of apoptotic cells (P<0.05). Conclusion: The results of this study reveal a potential of atorvastatin as an effective antiasthmatic agent by reducing IL-13-induced lung inflammation via the modulation of macrophage polarization. (Allergy Asthma Respir Dis 2021;9:76-83)