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FSH1 调控致病性皮肤癣菌须毛癣菌的表型和致病性。

FSH1 regulates the phenotype and pathogenicity of the pathogenic dermatophyte Microsporum canis.

机构信息

Department of Dermatology, The First Affiliated Hospital of Dalian Medical University, Chengdu, Sichuan 11736, P.R. China.

Department of Dermatology, Hospital of Anjing Town, Chengdu, Sichuan 11736, P.R. China.

出版信息

Int J Mol Med. 2019 Dec;44(6):2047-2056. doi: 10.3892/ijmm.2019.4355. Epub 2019 Sep 27.

DOI:10.3892/ijmm.2019.4355
PMID:31573050
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6844631/
Abstract

Microsporum canis (M. canis) is a common pathogen that causes tinea capitis and is present worldwide. The incidence of M. canis infection, particularly tinea capitis, has been increasing in China. In our previous studies, family of serine hydrolases 1 (FSH1) was identified as a potential virulence factor in tinea capitis infection caused by M. canis. To determine the function of this gene in M. canis, FSH1 was knocked down using double‑stranded RNA interference mediated by Agrobacterium tumefaciens. Reverse transcription‑quantitative PCR analysis was used to confirm gene knockdown. Loss of FSH1 expression by RNAi resulted in a minor phenotype alteration, but M. canis pathogenicity in guinea pig cutaneous infection was decreased compared with the wild‑type strain. To the best of our knowledge, the present study is the first to demonstrate that FSH1 is associated with macroconidia septa formation and is an important contributor to M. canis virulence. These findings may advance the understanding of the function of the FSH1 gene and provide a foundation for future studies on macroconidia septa formation and pathogenicity of M. canis.

摘要

犬小孢子菌(M. canis)是一种常见的病原体,可引起头癣,分布于世界各地。在中国,犬小孢子菌感染(尤其是头癣)的发病率一直在上升。在我们之前的研究中,丝氨酸水解酶家族 1(FSH1)被鉴定为犬小孢子菌引起的头癣感染的一个潜在毒力因子。为了确定该基因在犬小孢子菌中的功能,我们使用农杆菌介导的双链 RNA 干扰技术对 FSH1 进行了敲低。采用反转录-定量 PCR 分析来验证基因敲低。通过 RNAi 敲低 FSH1 的表达导致表型轻微改变,但与野生型菌株相比,犬小孢子菌对豚鼠皮肤感染的致病性降低。据我们所知,本研究首次证明 FSH1 与大分生孢子隔膜形成有关,是犬小孢子菌毒力的重要贡献者。这些发现可能有助于深入了解 FSH1 基因的功能,并为未来犬小孢子菌大分生孢子隔膜形成和致病性的研究提供基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/9018812ff188/IJMM-44-06-2047-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/d22839a8a2a1/IJMM-44-06-2047-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/6ac7d077b784/IJMM-44-06-2047-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/8fc0ddf62ba6/IJMM-44-06-2047-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/e734451a77eb/IJMM-44-06-2047-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/72ab5e4f16cf/IJMM-44-06-2047-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/2dcecb191141/IJMM-44-06-2047-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/9018812ff188/IJMM-44-06-2047-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/d22839a8a2a1/IJMM-44-06-2047-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/6ac7d077b784/IJMM-44-06-2047-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/8fc0ddf62ba6/IJMM-44-06-2047-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/e734451a77eb/IJMM-44-06-2047-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/72ab5e4f16cf/IJMM-44-06-2047-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/2dcecb191141/IJMM-44-06-2047-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0d5/6844631/9018812ff188/IJMM-44-06-2047-g06.jpg

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