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分化的 C2C12 肌肉细胞的存在增强了 A 型菌株 ATCC3624 的毒素产生和生长。

The presence of differentiated C2C12 muscle cells enhances toxin production and growth by type A strain ATCC3624.

机构信息

Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.

出版信息

Virulence. 2024 Dec;15(1):2388219. doi: 10.1080/21505594.2024.2388219. Epub 2024 Aug 27.

DOI:10.1080/21505594.2024.2388219
PMID:39192628
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11364075/
Abstract

type A causes gas gangrene, which involves muscle infection. Both alpha toxin (PLC), encoded by the gene, and perfringolysin O (PFO), encoded by the gene, are important when type A strains cause gas gangrene in a mouse model. This study used the differentiated C2C12 muscle cell line to test the hypothesis that one or both of those toxins contributes to gas gangrene pathogenesis by releasing growth nutrients from muscle cells. RT-qPCR analyses showed that the presence of differentiated C2C12 cells induces type A strain ATCC3624 to upregulate and expression, as well as increase expression of several regulatory genes, including , , and . The VirS/R two component regulatory system (TCRS) and its coupled Agr-like quorum sensing system, along with the EutV/W TCRS (which regulates expression of genes involved in ethanolamine [EA] utilization), were shown to mediate the C2C12 cell-induced increase in and expression. EA was demonstrated to increase toxin gene expression. ATCC3624 growth increased in the presence of differentiated C2C12 muscle cells and this effect was shown to involve both PFO and PLC. Those membrane-active toxins were each cytotoxic for differentiated C2C12 cells, suggesting they support ATCC3624 growth by releasing nutrients from differentiated C2C12 cells. These findings support a model where, during gas gangrene, increased production of PFO and PLC in the presence of muscle cells causes more damage to those host cells, which release nutrients like EA that are then used to support growth in muscle.

摘要

A型引起气性坏疽，涉及肌肉感染。在 A 型菌株引起小鼠气性坏疽模型中，α毒素（PLC）和产气荚膜梭菌溶细胞素 O（PFO）都非常重要，这两种毒素均由 基因编码。本研究使用分化的 C2C12 肌细胞系来验证假设，即这两种毒素之一或两者均通过从肌细胞释放生长营养物质而有助于气性坏疽发病机制。RT-qPCR 分析表明，分化的 C2C12 细胞的存在诱导 A 型菌株 ATCC3624 上调 和 表达，以及增加几种调节基因的表达，包括 、 、 。VirS/R 双组分调节系统（TCRS）及其偶联的 Agr 样群体感应系统，以及 EutV/W TCRS（调节参与乙醇胺 [EA] 利用的基因的表达），被证明介导 C2C12 细胞诱导的 和 表达增加。证明 EA 增加毒素基因表达。在分化的 C2C12 肌细胞存在的情况下，ATCC3624 生长增加，并且这种作用涉及 PFO 和 PLC。这些膜活性毒素对分化的 C2C12 细胞均具有细胞毒性，这表明它们通过从分化的 C2C12 细胞释放营养物质来支持 ATCC3624 的生长。这些发现支持这样的模型，即在气性坏疽期间，肌肉细胞存在时 PFO 和 PLC 的产量增加会对这些宿主细胞造成更大的损害，从而释放出 EA 等营养物质，然后这些营养物质被用于支持肌肉中 的生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/f153115f948a/KVIR_A_2388219_F0009_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/6a1b57aef6b6/KVIR_A_2388219_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/d37c5d66237a/KVIR_A_2388219_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/4d993fc52a49/KVIR_A_2388219_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/9a52fee52238/KVIR_A_2388219_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/ae941e6eea34/KVIR_A_2388219_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/427ada18ae6f/KVIR_A_2388219_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/3005c4d75605/KVIR_A_2388219_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/4c3296159ac6/KVIR_A_2388219_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/f153115f948a/KVIR_A_2388219_F0009_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/6a1b57aef6b6/KVIR_A_2388219_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/d37c5d66237a/KVIR_A_2388219_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/4d993fc52a49/KVIR_A_2388219_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/9a52fee52238/KVIR_A_2388219_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/ae941e6eea34/KVIR_A_2388219_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/427ada18ae6f/KVIR_A_2388219_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/3005c4d75605/KVIR_A_2388219_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/4c3296159ac6/KVIR_A_2388219_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab57/11364075/f153115f948a/KVIR_A_2388219_F0009_OC.jpg

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