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Chung-Yu Lan 2 Articles
Contribution of EmrAB efflux pumps to colistin resistance in Acinetobacter baumannii
Ming-Feng Lin , Yun-You Lin , Chung-Yu Lan
J. Microbiol. 2017;55(2):130-136.   Published online January 26, 2017
DOI: https://doi.org/10.1007/s12275-017-6408-5
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AbstractAbstract PDF
Efflux pumps play an important role in antimicrobial resistance for Acinetobacter baumannii. However, the function of the Emr pump system and the relationship between Emr and drug resistance has not been characterized in A. baumannii. In this study, four possible groups of emr-like genes were found by searching a genome database. Among them, A1S_ 1772 (emrB) and A1S_1773 (emrA) were demonstrated to be co-transcribed as a single operon. Moreover, during osmotic stress, A1S_1772 showed the largest change in gene expression compared to the other emrB-like genes, and deletion of A1S_1772 (AB ΔemrB) significantly slowed cell growth in 20% sucrose. Using a phenotypic microarray analysis, the AB ΔemrB mutant was more susceptible to colistin and nafcillin, paromomycin, spiramycin, and D,L-serine hydroxmate than the wild type. The spot assay, time kill assay and minimal inhibition concentration determination also indicated that the wild type could tolerate colistin better than the AB ΔemrB mutant. Finally, the increased expression levels of all emrBlike genes, including A1S_0775, A1S_0909, A1S_1772, and A1S_1799, in colistin resistance-induced A. baumannii further supported the possible involvement of the emrB genes in A. baumannii colistin resistance. Together, the Emr pump systems in A. baumannii contribute to adaptation to osmotic stress and resistance to colistin.

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Responses of Candida albicans to the Human Antimicrobial Peptide LL-37
Pei-Wen Tsai , Yin-Lien Cheng , Wen-Ping Hsieh , Chung-Yu Lan
J. Microbiol. 2014;52(7):581-589.   Published online May 30, 2014
DOI: https://doi.org/10.1007/s12275-014-3630-2
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AbstractAbstract PDF
Candida albicans is a major fungal pathogen in humans. Antimicrobial peptides (AMPs) are critical components of the innate immune response in vertebrates and represent the first line of defense against microbial infection. LL-37 is the only member of the human family of cathelicidin AMPs and is commonly expressed by various tissues and cells, including surfaces of epithelia. The candidacidal effects of LL-37 have been well documented, but the mechanisms by which LL-37 kills C. albicans are not completely understood. In this study, we examined the effects of LL-37 on cell wall and cellular responses in C. albicans. Using transmission electron microscopy, carbohydrate analyses, and staining for β-1,3-glucan, changing of C. albicans cell wall integrity was detected upon LL-37 treatment. In addition, LL-37 also affected cell wall architecture of the pathogen. Finally, DNA microarray analysis and quantitative PCR demonstrated that sub-lethal concentrations of LL-37 modulated the expression of genes with a variety of functions, including transporters, regulators for biological processes, response to stress or chemical stimulus, and pathogenesis. Together, LL-37 induces complex responses in C. albicans, making LL-37 a promising candidate for use as a therapeutic agent against fungal infections.

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