Chen Fengjia, Zhang Jing, Ji Hyun Jung, Kim Min-Kyu, Kim Kyoung Whun, Choi Jong-Il, Han Seung Hyun, Lim Sangyong, Seo Ho Seong, Ahn Ki Bum
Research Division for Radiation Science, Korea Atomic Energy Research Institute, Jeongeup, South Korea.
Department of Biotechnology and Bioengineering, Chonnam National University, Gwangju, South Korea.
Front Microbiol. 2021 Dec 24;12:712086. doi: 10.3389/fmicb.2021.712086. eCollection 2021.
is an extremely resistant bacterium against extracellular stress owing to on its unique physiological functions and the structure of its cellular constituents. Interestingly, it has been reported that the pattern of alteration in proportion on the skin is negatively correlated with skin inflammatory diseases, whereas the proportion of was increased in patients with chronic skin inflammatory diseases. However, the biological mechanisms of deinococcal interactions with other skin commensal bacteria have not been studied. In this study, we hypothesized that deinococcal cellular constituents play a pivotal role in preventing colonization by inhibiting biofilm formation. To prove this, we first isolated cellular constituents, such as exopolysaccharide (DeinoPol), cell wall (DeinoWall), and cell membrane (DeinoMem), from and investigated their inhibitory effects on colonization and biofilm formation and . Among them, only DeinoPol exhibited an anti-biofilm effect without affecting bacterial growth and inhibiting staphylococcal colonization and inflammation in a mouse skin infection model. Moreover, the inhibitory effect was impaired in the Δ strain, a mutant that cannot produce DeinoPol. Remarkably, DeinoPol not only interfered with biofilm formation at early and late stages but also disrupted a preexisting biofilm by inhibiting the production of poly--acetylglucosamine (PNAG), a key molecule required for biofilm formation. Taken together, the present study suggests that DeinoPol is a key molecule in the negative regulation of biofilm formation by . Therefore, DeinoPol could be applied to prevent and/or treat infections or inflammatory diseases associated with biofilms.
由于其独特的生理功能和细胞成分结构，是一种对细胞外应激具有极强抵抗力的细菌。有趣的是，据报道，其在皮肤上比例的变化模式与皮肤炎症性疾病呈负相关，而在慢性皮肤炎症性疾病患者中其比例增加。然而，嗜皮菌与其他皮肤共生细菌相互作用的生物学机制尚未得到研究。在本研究中，我们假设嗜皮菌细胞成分通过抑制生物膜形成在预防[未提及的细菌]定殖中起关键作用。为了证明这一点，我们首先从[嗜皮菌]中分离出细胞成分，如胞外多糖（DeinoPol）、细胞壁（DeinoWall）和细胞膜（DeinoMem），并研究它们对[未提及的细菌]定殖和生物膜形成的抑制作用。其中，只有DeinoPol表现出抗生物膜作用，且不影响细菌生长，并在小鼠皮肤感染模型中抑制葡萄球菌定殖和炎症。此外，在不能产生DeinoPol的突变体Δ菌株中，抑制作用受损。值得注意的是，DeinoPol不仅在早期和晚期干扰[未提及的细菌]生物膜形成，还通过抑制[未提及的细菌]生物膜形成所需的关键分子聚-N-乙酰葡糖胺（PNAG）的产生来破坏预先存在的生物膜。综上所述，本研究表明DeinoPol是[未提及的细菌]对[未提及的细菌]生物膜形成负调控的关键分子。因此，DeinoPol可用于预防和/或治疗与[未提及的细菌]生物膜相关的感染或炎症性疾病。
