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Mei-Hui Lin

Mei-Hui Lin

JobTitle: Associate Professor

CurrentJob: Associate Professor

E-mail: thea@mail.cgu.edu.tw

Phone: 5206 3433

Education: Ph. D., Microbiology, Chang Gung University, Taiwan

Expertise: Clinical Microbiology, Bacteriology

Website: https://sites.google.com/view/cgu-mhl--lab/

Lab & Research Interest

Staphylococcus aureus is an important nosocomial and community-associated pathogen that causes a variety of human diseases. My studies are interested in the multicellular behaviors and pathogenesis of S. aureus. My research topics include:

(A)    Molecular mechanisms of colony spreading. 
Staphylococcus aureus is known to form giant colonies on the soft agar medium by a process called colony spreading. To identify the genes that are required for colony spreading, I mutagenized S. aureus with a mariner-based transposon, bursa aurealis. The genes that are involved in colony spreading are under investigation.

(B)    Interactions between S. aureus and host cells. 

(C)    Functional analysis of a virulence factor PrsA. 
PrsA is an extracytoplasmic lipoprotein which regulates late phase protein secretion. However the role of PrsA in S. aureus is notclear. To investigate the functions of PrsA in S. aureus, we constructed a prsA knockout strain (ΔprsA).Exoprotein analysis revealed that PrsA influences several exoproteins secretion. The results from a mouse model of intravenous infection and phagocytosis assay also indicated that PrsA is involved in virulence and pathogenesis of S. aureus. The mechanisms involved in PrsA-mediated pathogenesis are further investigated.

(D)    Mechanisms of Reduced Vancomycin Susceptibility in Staphylococcus aureus

(E)    Virulence analysis of Staphylococcus lugdunensis
Investigating the virulence factors of S. lugdunesis using transposon mutagenesis and Caenorhabditis elegans infection model.

 

Publication

1.  CC Liu, SC Chang, JC Shu, MH Lin#. 2025. Defects in energy metabolism increase the susceptibility of Staphylococcus aureus and its small colony variants (SCVs) to Staphylococcus lugdunensis and lugdunin. Microbiology Spectrum. 13:e0100625. 

2.  MH Lin#, CC Liu, CW Lu and JC Shu. 2024. Staphylococcus aureus foldase PrsA contributes to the folding and secretion of protein A. BMC Microbiology, 24:108. 

3.  CC Liu and MH Lin#. 2023. Hitchhiking motility of Staphylococcus aureus involves the interaction between its wall teichoic acids and lipopolysaccharide of Pseudomonas aeruginosa. Frontiers in Microbiology, 13:1068251. 

4.  CC Liu and MH Lin#. 2020. Involvement of Heme in Colony Spreading of Staphylococcus aureus. Frontiers in Microbiology, 11, 170. 

5.  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. 

6.  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 Microbiology. 17:92.

7.  MH Lin#, WJ Ke, CC Liu, MW Yang. 2016. Modulation of Staphylococcus aureus spreading by water. Scientific Reports 6:25233. 

8.  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. 

9.  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.