Proteomic Adaptation of Streptococcus pneumoniae to the Antimicrobial Peptide Human Beta Defensin 3 (hBD3) in Comparison to Other Cell Surface Stresses.
Proteomic Adaptation of Streptococcus pneumoniae to the Antimicrobial Peptide Human Beta Defensin 3 (hBD3) in Comparison to Other Cell Surface Stresses.
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肺炎链球菌对抗菌肽人β防御素3(HBD3)的蛋白质组适应与其他细胞表面应激的比较。
DOI：
10.3390/microorganisms8111697
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发表时间：
2020-10-30
期刊：
影响因子：
4.5
通讯作者：
Becher D
中科院分区：
文献类型：
--
作者：
Mücke PA;Ostrzinski A;Hammerschmidt S;Maaß S;Becher D
抗菌肽人β防御素3(HBD3)是先天免疫系统的重要组成部分，通过特异地渗透细菌膜来保护呼吸道病原体。革兰氏阳性菌肺炎链球菌会导致严重的疾病，包括肺炎、脑膜炎和败血症，尽管在定植和感染期间经常接触包括hBD3在内的人类防御分子。因此，问题产生了肺炎球菌如何适应由抗菌肽引起的压力。我们通过分析hBD3处理后肺炎链球菌的蛋白质组来解决这个问题，并将我们的数据与存在于人类呼吸道中的另一种关键抗菌肽LL-37诱导的蛋白质组变化进行比较。由于抗菌肽通常会引起膜的扰动，因此研究了膜活性阳离子洗涤剂十六烷基三甲基溴化铵(CTAB)对肺炎球菌抗菌肽反应的特异性。简而言之，hBD3和LL-37在肺炎球菌中引起类似的反应，特别是带有注释的转运蛋白和毒力功能的蛋白的变化已经被识别。然而，LL-37引起细胞表面修饰蛋白丰度的变化，这在hBD3处理后无法观察到。有趣的是，CTAB诱导肺炎链球菌发生独特的蛋白质组变化。然而，洗涤剂似乎激活了一个双组分系统，该系统也是在抗菌肽压力下激活的(TCS 05)。总体而言，我们的数据代表了肺炎球菌在功能水平上对特定细胞表面压力的适应的新资源。这一知识可能被用来开发策略，以规避肺炎球菌对抗菌肽的耐药性。
The antimicrobial peptide human Beta defensin 3 (hBD3) is an essential part of the innate immune system and is involved in protection against respiratory pathogens by specifically permeabilizing bacterial membranes. The Gram-positive bacterium Streptococcus pneumoniae causes serious diseases including pneumonia, meningitis, and septicemia, despite being frequently exposed to human defense molecules, including hBD3 during colonization and infection. Thus, the question arises how pneumococci adapt to stress caused by antimicrobial peptides. We addressed this subject by analyzing the proteome of S. pneumoniae after treatment with hBD3 and compared our data with the proteomic changes induced by LL-37, another crucial antimicrobial peptide present in the human respiratory tract. As antimicrobial peptides usually cause membrane perturbations, the response to the membrane active cationic detergent cetyltrimethylammonium bromide (CTAB) was examined to assess the specificity of the pneumococcal response to antimicrobial peptides. In brief, hBD3 and LL-37 induce a similar response in pneumococci and especially, changes in proteins with annotated transporter and virulence function have been identified. However, LL-37 causes changes in the abundance of cell surface modification proteins that cannot be observed after treatment with hBD3. Interestingly, CTAB induces unique proteomic changes in S. pneumoniae. Though, the detergent seems to activate a two-component system that is also activated in response to antimicrobial peptide stress (TCS 05). Overall, our data represent a novel resource on pneumococcal adaptation to specific cell surface stresses on a functional level. This knowledge can potentially be used to develop strategies to circumvent pneumococcal resistance to antimicrobial peptides.
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影响因子：
3.1
作者：
Melin, Merit;Di Paolo, Emmanuel;Vakevainen, Merja
通讯作者：
Vakevainen, Merja
影响因子：
4.4
作者：
Cox, Juergen;Neuhauser, Nadin;Mann, Matthias
通讯作者：
Mann, Matthias
影响因子：
5.2
作者：
Hashemi, Marjan M.;Holden, Brett S.;Savage, Paul B.
通讯作者：
Savage, Paul B.
影响因子：
3.2
作者：
Damjanovic, Marlen;Kharat, Arun S.;Vollmer, Waldemar
通讯作者：
Vollmer, Waldemar
影响因子：
3.7
作者：
Cole JN;Nizet V
通讯作者：
Nizet V