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非生物膜形成共生表皮葡萄球菌分离株在胰蛋白酶存在的情况下产生生物膜。

Non-biofilm-forming commensal Staphylococcus epidermidis isolates produce biofilm in the presence of trypsin.

机构信息

Laboratory of Immunomicrobiology, Department of Microbiology, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Mexico City, Mexico.

Laboratory of Infectology, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Mexico City, Mexico.

出版信息

Microbiologyopen. 2019 Oct;8(10):e906. doi: 10.1002/mbo3.906. Epub 2019 Aug 7.

Abstract

Epidemiological studies comparing clinical and commensal Staphylococcus epidermidis isolates suggest that biofilm formation is a discriminant biomarker. A study showed that four non-biofilm-forming clinical S. epidermidis isolates could form an induced biofilm by trypsin treatment, suggesting that S. epidermidis can form biofilms in a protease-independent way and in a trypsin-induced way. In this study, the trypsin capacity to induce biofilm formation was evaluated in non-biofilm-forming S. epidermidis isolates (n = 133) in order to support this mechanism and to establish the importance of total biofilms (meaning the sum of protease-independent biofilm and trypsin-induced biofilm). Staphylococcus epidermidis isolates from ocular infections (OI; n = 24), prosthetic joint infections (PJI; n = 64), and healthy skin (HS-1; n = 100) were screened for protease-independent biofilm formation according to Christensen's method. The result was that there are significant differences (p < .0001) between clinical (43.2%) and commensal (17%) protease-independent biofilm producers. Meanwhile, non-biofilm-forming isolates were treated with trypsin, and biofilm formation was evaluated by the same method. The number of commensal trypsin-induced biofilm producers significantly increased from 17% to 79%. In contrast, clinical isolates increased from 43.2% to 72.7%. The comparison between clinical and commensal total biofilm yielded no significant differences (p = .392). A similar result was found when different isolation sources were compared (OI vs. HS-1 and PJI vs. HS-1). The genotype icaA /aap was associated with the trypsin-induced biofilm phenotype; however, no correlation was observed between aap mRNA expression and the level of trypsin-induced biofilm phenotype. Studying another group of commensal S. epidermidis non-biofilm-forming isolates (HS-2; n = 139) from different body sites, it was found that 70 isolates (60.3%) formed trypsin-induced biofilms. In conclusion, trypsin is capable of inducing biofilm production in non-biofilm-forming commensal S. epidermidis isolates with the icaA /aap genotype, and there is no significant difference in total biofilms when comparing clinical and commensal isolates, suggesting that total biofilms are not a discriminant biomarker.

摘要

比较临床和共生表皮葡萄球菌分离株的流行病学研究表明,生物膜形成是一个有区别的生物标志物。一项研究表明,四种非生物膜形成的临床表皮葡萄球菌分离株可以通过胰蛋白酶处理形成诱导生物膜,这表明表皮葡萄球菌可以通过非蛋白酶依赖的方式和胰蛋白酶诱导的方式形成生物膜。在这项研究中,评估了非生物膜形成的表皮葡萄球菌分离株(n=133)中胰蛋白酶诱导生物膜形成的能力,以支持这一机制,并确定总生物膜(即独立于蛋白酶的生物膜和胰蛋白酶诱导的生物膜之和)的重要性。筛选眼感染(OI;n=24)、人工关节感染(PJI;n=64)和健康皮肤(HS-1;n=100)的表皮葡萄球菌分离株是否具有独立于蛋白酶的生物膜形成能力,根据 Christensen 的方法进行。结果表明,临床(43.2%)和共生(17%)蛋白酶独立生物膜生产者之间存在显著差异(p<.0001)。同时,用胰蛋白酶处理非生物膜形成的分离株,并通过相同的方法评估生物膜形成。共生的胰蛋白酶诱导生物膜生产者的数量从 17%显著增加到 79%。相比之下,临床分离株的比例从 43.2%增加到 72.7%。临床和共生总生物膜之间的比较没有显著差异(p=0.392)。当比较不同的分离源(OI 与 HS-1 和 PJI 与 HS-1)时,也得到了类似的结果。icaA/aap 基因型与胰蛋白酶诱导的生物膜表型相关;然而,aap mRNA 表达水平与胰蛋白酶诱导的生物膜表型之间没有相关性。在研究另一组来自不同身体部位的非生物膜形成的共生表皮葡萄球菌分离株(HS-2;n=139)时,发现 70 株(60.3%)形成了胰蛋白酶诱导的生物膜。总之,胰蛋白酶能够诱导具有 icaA/aap 基因型的非生物膜形成的共生表皮葡萄球菌分离株产生生物膜,并且在比较临床和共生分离株时,总生物膜没有显著差异,这表明总生物膜不是一个有区别的生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d26/6813491/dea31bb9d561/MBO3-8-e906-g001.jpg

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