Nucleotide Messenger Signaling of Staphylococci in Responding to Nitric Oxide - Releasing Biomaterials.
Nucleotide Messenger Signaling of Staphylococci in Responding to Nitric Oxide - Releasing Biomaterials.
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DOI：
10.1021/acsbiomaterials.2c01536
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发表时间：
2023-06-12
影响因子：
5.8
通讯作者：
Xu, Li-Chong
中科院分区：
文献类型：
--
作者：
Ochetto, Alyssa;Sun, Dongxiao;Siedlecki, Christopher A.;Xu, Li-Chong
一氧化氮(NO)释放生物材料是治疗医疗器械相关微生物感染的一种很有前途的方法。与高浓度的NO杀菌作用不同，低浓度的NO是抑制生物膜形成或分散成熟生物膜的重要信号分子，它通过调节许多革兰氏阴性菌的细胞内核苷酸第二信使网络，如环二聚鸟苷(c-di-GMP)，来抑制生物膜的形成或分散成熟的生物膜。然而，革兰氏阳性葡萄球菌是留置设备上最常见的微生物感染，但对核苷酸信使及其对NO的反应以及NO抑制生物被膜形成的机制知之甚少。研究了金黄色葡萄球菌纽曼D2C和表皮葡萄球菌RP62a与S-亚硝基-N-乙酰青霉胺(SNAP，NO供体)浸渍的聚氨酯(PU)膜孵育后，环核苷酸第二信使c-di-GMP、环二聚体一磷酸腺苷(c-di-AMP)和环一磷酸(CAMP)的变化。结果表明，聚合物膜释放的NO显著降低了金黄色葡萄球菌浮游细胞和固着细胞中c-di-GMP的水平，这些细菌表现出抑制生物被膜的形成。然而，NO释放对表皮葡萄球菌c-di-GMP的影响很小，但表皮葡萄球菌对NO释放的反应表现为c-di-AMP水平显著降低，生物被膜形成减少。结果强烈表明，对于这两种细菌，NO以不同的方式调节核苷酸第二信使信号网络，但对于这两种细菌，这些信号的变化影响生物膜的形成。这些发现为理解NO抑制葡萄球菌生物被膜的机制提供了线索，并为抗生物被膜干预提供了新的靶点。
Nitric oxide (NO) releasing biomaterials are a promising approach against medical device associated microbial infection. In contrast to the bacteria-killing effects of NO at high concentrations, NO at low concentrations serves as an important signaling molecule to inhibit biofilm formation or disperse mature biofilms by regulating the intracellular nucleotide second messenger signaling network such as cyclic dimeric guanosine monophosphate (c-di-GMP) for many Gram-negative bacterial strains. However, Gram-positive staphylococcal bacteria are the most commonly diagnosed microbial infections on indwelling devices, but much less is known about the nucleotide messengers and their response to NO as well as the mechanism by which NO inhibits biofilm formation. This study investigated the cyclic nucleotide second messengers c-di-GMP, cyclic dimeric adenosine monophosphate (c-di-AMP), and cyclic adenosine monophosphate (cAMP) in both Staphylococcus aureus (S. aureus) Newman D2C and Staphylococcus epidermidis (S. epidermidis) RP62A after incubating with S-nitroso-N-acetylpenicillamine (SNAP, NO donor) impregnated polyurethane (PU) films. Results demonstrated that NO release from the polymer films significantly reduced the c-di-GMP levels in S. aureus planktonic and sessile cells, and these bacteria showed inhibited biofilm formation. However, the effect of NO release on c-di-GMP in S. epidermidis was weak, but rather, S. epidermidis showed significant reduction in c-di-AMP levels in response to NO release and also showed reduced biofilm formation. Results strongly suggest that NO regulates the nucleotide second messenger signaling network in different ways for these two bacteria, but for both bacteria, these changes in signaling affect the formations of biofilms. These findings provide cues to understand the mechanism of Staphylococcus biofilm inhibition by NO and suggest novel targets for antibiofilm interventions.
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