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林美惠副教授

林 美 惠 (Mei-Hui Lin)

學歷

長庚大學生物醫學研究所博士

任課科目

臨床微生物學與實驗、高等細菌學、細胞生物學

研究專長

臨床細菌學、細菌生物膜、細菌致病機制、細菌與寄主之互動關係

辦公室分機

5206

實驗室分機

3433

個人網頁

臨床細菌暨細菌遺傳學研究室

E-mail

theamail.cgu.edu.tw

研究方向及研究室特色(Lab & Research Interest)

本實驗室以臨床上重要之致病菌金黃色葡萄球菌為主要研究對象,探討主題包括:

(I)  金黃色葡萄球菌之多細胞行為

A. 生物膜 (Biofilm)

金黃色葡萄球菌是很重要的院內感染以及社區感染的病原菌,常引起人類的多種疾病。金黃色葡萄球菌容易在醫療裝置上產生細菌生物膜是引發慢性細菌性感染的主因之一,而生長在生物膜內的細菌具有比較高的抗藥性也更能抵抗宿主免疫系統,這使得此類感染的治療更加困難。因此本研究室主要在探討金黃色葡萄球菌形成生物膜的機制

B. 擴散運動 (Spreading)

細菌常具有群聚運動之行為,包括 swarming, swimming, sliding and spreading, 這些集體運動行為常和致病性相關;大部分具有運動行為的細菌具有鞭毛或纖毛等結構幫助其移動,而金黃色葡萄球菌為不具有鞭毛或纖毛之球菌,本研究室主要在探討其如何進行群體運動以及和致病性有何相關性。

(II) 金黃色葡萄球菌之致病機制

A. 宿主細胞與細菌之互動關係

當細菌感染人體時可能引發宿主細胞免疫反應以及細菌如何躲避免疫系統之攻擊亦是本實驗室有興趣之主題。

B. 金黃色葡萄球菌之毒性基因與致病機制

致病性金黃色葡萄球菌會產生多種毒素而造成不同之疾病,其毒性基因之表現與致病力息息相關,本實驗室利用細胞模式及動物實驗觀察毒性基因表現與致病力之相關性。

(III) 金黃色葡萄球菌之抗藥機制

      探討對萬古黴素中度抗性之金黃色葡萄球菌(vancomycin-intermediate S. aureus, VISA) 的抗藥機制。

(IV) 路鄧氏葡萄球菌的毒性分析

       利用跳躍子隨機突變法和線蟲感染模式分析路鄧氏葡萄球菌的毒性因子

論文與著作(Publication)

Research articles:

  1. MH Lin, CC Li, JC Shu, HW Chu, CC Liu, and CC Wu. 2018. Exoproteome Profiling Reveals the Involvement of the Foldase PrsA in the Cell Surface Properties and Pathogenesis of Staphylococcus aureus. Proteomics. 18 (5-6): e1700195 [ SCI]
  2. HY Chen, MH Lin, CC Chen, JC Shu. 2017. The expression of fibronectin is significantly suppressed in macrophages to exert a protective effect against Staphylococcus aureus infection. BMC Microbiol. 17:92. [ SCI]
  3. MH Lin*, WJ Ke, CC Liu, MW Yang. 2016. Modulation of Staphylococcus aureus spreading by water. Scientific Reports 6:25233. (*correspondence) [ SCI]
  4. MH Lin, JC Shu, LP Lin, KY Chong, YW Cheng1, JF Du, ST Liu. 2015. Elucidating the crucial role of Poly N-acetylglucosamine from Staphylococcus aureus in cellular adhesion and pathogenesis. PLoS ONE 10:e0124216.
  5. CY Hsu*, JC Shu*, MH Lin, KYu Chong, CC Chen, SM Wen, YT Hsieh, WT Liao. 2015. High Glucose Concentration Promotes Vancomycin-Enhanced Biofilm Formation of Vancomycin -Non-Susceptible Staphylococcus aureus in Diabetic Mice. PLoS ONE 10:e0134852. (*Contribution equally) [ SCI]
  1. CJ Chen, MH Lin, JC Shu, JJ Lu. 2014. Reduced susceptibility to vancomycin in isogenic Staphylococcus aureus strains of sequence type 59: Tracking evolution and identifying mutations by whole-genome sequencing. Journal of Antimicrobial Chemotherapy 69:349-354. [SCI]
  2. YT Hsieh#, MH Lin#, HY Ho, CC Chen, LC Chen, JC Shu. 2013. Glucose-6-phosphate dehydrogenase (G6PD)-deficient epithelial cells are less tolerant to infection by Staphylococcus aureus. PLoS ONE  8:e79566. ( #Contribution equally) [ SCI]
  3. 6.  MH Lin, JF Fu and ST Liu. 2013. A repeat 1 sequence causes competition of ColE1-type plasmids. PLoS ONE  8:e61668 [ SCI]
  4. MH Lin *, Shu JC, HY Huang and YC Chang. 2012. Involvement of iron in biofilm formation by Staphylococcus aureus. PLoS ONE 7:e34388 (*correspondence) [ SCI]
  5. CY Hsu #, MH Lin#, CC Chen, SC Chien, YH Cheng, IN Su, JC Shu. 2011. Vancomycin promotes the bacterial autolysis, release of extracellular DNA, and biofilm formation in vancomycin-non - susceptible Staphylococcus aureus. FEMS Immunology & Medical Microbiology. 1:1-12 ( #Contribution equally) [ SCI]
  6. MH Lin, FR Chang, MY Hua and S.T. Liu., 2011. ”Inhibitory effect of   1,2,3,4,6-penta-O-galloyl-β-D-glucopyranose on biofilm formation by Staphylococcus aureus”, Antimicrobial Agents &Chemotherapy. 55:1021-7. [SCI]
  7. HY Chen, CC Chen, CS Fang, YT Hsieh, MH Lin, and JC Shu. 2011. “Vancomycin activates σB in vancomycin-resistant Staphylococcus aureus resulting in the enhancement of cytotoxicity”. PLoS ONE. 6:e24472. [ SCI]

Patents:

1. MH Lin, FR Chang, MY Hua, HW Yang and ST Liu. Inhibition of biofilm formation by 1,2,3,4,6-penta-o-galloyl-D-glucopyranose. United States Patent. (Patent No: US 9,181,290 B2) (Patent Period: Nov. 10, 2015 – Jan. 29, 2032)

2. 林美惠、張芳榮、華沐怡、楊閎蔚、劉世東. 利用1,2,3,4,6-五-O-沒食子醯基-D-葡      喃糖來抑制生物膜形成. 中華民國專利。專利案號: I-415572,專利權期: 20131121日至2031616

 

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