Kim Yong-Guy, Lee Jin-Hyung, Lee Jintae
School of Chemical Engineering, Yeungnam University, 280 Daehak-Ro, Gyeongsan 38541, Republic of Korea.
School of Chemical Engineering, Yeungnam University, 280 Daehak-Ro, Gyeongsan 38541, Republic of Korea.
Phytomedicine. 2021 Oct;91:153710. doi: 10.1016/j.phymed.2021.153710. Epub 2021 Aug 18.
Cutibacterium acnes is a major colonizer and inhabitant of human skin and contributes to the pathogenesis of acne vulgaris. C. acnes either alone or with Staphylococcus aureus, which also inhabits skin, readily forms biofilms that are often tolerant of conventional antibiotics and the host immune system. It was hypothesized that the amphiphilic nature of some fatty acids (FAs) inhibit C. acnes or mixed biofilm formation.
The antibacterial and antibiofilm activities of 24 saturated and unsaturated FAs were investigated against C. acnes as well as a mixture of the bacteria C. acnes and S. aureus.
Anti-biofilm assays, antimicrobial assays, confocal laser scanning microscopy, scanning electron microscopy, extracellular polymeric substance production, and microbial adherence to hydrocarbon assay were utilized to elucidate how active FAs influence biofilm development.
Seventeen FAs at 20 µg/ml inhibited C. acnes biofilm formation by 60-99%. The minimum inhibitory concentrations (MICs) of 20 FAs were ≥ 500 µg/ml but 4 medium-chain FAs had MICs in a range 15 to 200 µg/ml. Interestingly, myristoleic acid inhibited biofilm formation at 1 μg/ml. Myristoleic acid also inhibited the formation of S. aureus and mixed C. acnes/S. aureus biofilms. FAs reduced C. acnes hydrophobicity and we found this was generally correlated with their antibiofilm forming efficacies. Transcriptional analyses showed that myristoleic acid modulates the expression of several biofilm-related genes such as lipase, hyaluronate lyase, and virulence-related genes.
This study shows myristoleic acid and other FAs inhibit biofilm formation by C. acnes and mixed biofilm formation by C. acnes and S. aureus. Hence, myristoleic acid might be useful for treating or preventing acne and C. acnes associated diseases.
痤疮丙酸杆菌是人类皮肤的主要定植菌和常驻菌,在寻常痤疮的发病机制中起作用。痤疮丙酸杆菌单独或与同样栖息于皮肤的金黄色葡萄球菌一起,很容易形成生物膜,这些生物膜通常对传统抗生素和宿主免疫系统具有耐受性。据推测,某些脂肪酸(FAs)的两亲性可抑制痤疮丙酸杆菌或混合生物膜的形成。
研究24种饱和和不饱和脂肪酸对痤疮丙酸杆菌以及痤疮丙酸杆菌与金黄色葡萄球菌混合物的抗菌和抗生物膜活性。
采用抗生物膜试验、抗菌试验、共聚焦激光扫描显微镜、扫描电子显微镜、胞外聚合物产生试验和微生物对碳氢化合物的粘附试验,以阐明活性脂肪酸如何影响生物膜的形成。
17种浓度为20μg/ml的脂肪酸可抑制痤疮丙酸杆菌生物膜形成60%-99%。20种脂肪酸的最低抑菌浓度(MICs)≥500μg/ml,但4种中链脂肪酸的MICs在15至200μg/ml范围内。有趣的是,肉豆蔻油酸在1μg/ml时即可抑制生物膜形成。肉豆蔻油酸还可抑制金黄色葡萄球菌以及痤疮丙酸杆菌/金黄色葡萄球菌混合生物膜的形成。脂肪酸降低了痤疮丙酸杆菌的疏水性,我们发现这通常与其抗生物膜形成功效相关。转录分析表明,肉豆蔻油酸可调节几个与生物膜相关的基因如脂肪酶、透明质酸裂解酶以及与毒力相关基因的表达。
本研究表明肉豆蔻油酸和其他脂肪酸可抑制痤疮丙酸杆菌生物膜形成以及痤疮丙酸杆菌与金黄色葡萄球菌的混合生物膜形成。因此,肉豆蔻油酸可能有助于治疗或预防痤疮及与痤疮丙酸杆菌相关的疾病。