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IgY 靶向种植体相关感染中的细菌群体感应分子。

IgY Targeting Bacterial Quorum-Sensing Molecules in Implant-Associated Infections.

机构信息

Center for Orthopedics, Trauma Surgery and Spinal Cord Injury, Heidelberg University Hospital, Schlierbacher Landstrasse 200a, 69118 Heidelberg, Germany.

Department of Anesthesiology, Heidelberg University Hospital, Im Neuenheimer Feld 672, 69120 Heidelberg, Germany.

出版信息

Molecules. 2020 Sep 3;25(17):4027. doi: 10.3390/molecules25174027.

Abstract

: Implant-associated infections are still a major complication in the field of orthopedics. Bacteria can form biofilms on implant surfaces, making them more difficult to detect and treat. Since standard antibiotic therapy is often impaired in biofilm infections, particular interest is directed towards finding treatment alternatives. Biofilm-formation is a well-organized process during which bacteria communicate via quorum-sensing molecules (QSM). The aim of this study was to inhibit bacterial communication by directing avian IgY against specific QSM. : Chicken were immunized against the following QSM: (1) AtlE, a member of the autolysin family which mediates attachment to a surface in ; (2) GroEL, the bacterial heat shock protein; (3) PIA (polysaccharide intercellular adhesion), which is essential for cell-cell adhesion in biofilms. biofilms were grown and inhibition of biofilm-formation by IgYs was evaluated. Additionally, human osteoblasts were cultivated and biocompatibility of IgYs was tested. : We were able to demonstrate that all IgYs reduced biofilm-formation, also without prior immunization. Therefore, the response was probably not specific with regard to the QSM. Osteoblasts were activated by all IgYs which was demonstrated by microscopy and an increased release of IL-8. : In conclusion, avian IgY inhibits biofilm-formation, though the underlying mechanism is not yet clear. However, adverse effects on local tissue cells (osteoblasts) were also observed.

摘要

植入物相关感染仍然是骨科领域的主要并发症。细菌可以在植入物表面形成生物膜,使其更难检测和治疗。由于标准抗生素治疗在生物膜感染中常常受到影响,因此特别关注寻找治疗替代品。生物膜形成是一个组织良好的过程,在此过程中细菌通过群体感应分子(QSM)进行通信。本研究的目的是通过针对特定 QSM 的禽类 IgY 来抑制细菌通信。

鸡被免疫针对以下 QSM:(1)AtlE,一种自溶素家族成员,介导与表面的附着;(2)GroEL,细菌热休克蛋白;(3)PIA(细胞间多糖黏附素),对生物膜中细胞-细胞黏附至关重要。

生物膜被生长并评估 IgY 对生物膜形成的抑制作用。此外,培养了人成骨细胞并测试了 IgY 的生物相容性。

我们能够证明所有 IgY 都减少了生物膜的形成,即使没有预先免疫也是如此。因此,反应可能不是针对 QSM 的特异性。所有 IgY 都激活了成骨细胞,这通过显微镜和 IL-8 释放增加得到证明。

总之,禽类 IgY 抑制生物膜形成,尽管其潜在机制尚不清楚。然而,也观察到对局部组织细胞(成骨细胞)的不良影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/270a/7504788/11cc58c52c7e/molecules-25-04027-g001.jpg

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