LH12 displayed stronger antibacterial activity against S. mutans at pH 5.5 with MICs ranging from 12.00 μg/mL to 64.00 μg/mL. Figure 2d.
- Measure
- MIC
- Value
- 12.00 μg/mL
- Target
- Streptococcus mutans
- Assay
- Not reported by source
Journal of Oral Microbiology · 2023
Sequence evidence
GLLHLLHHLLHHNH
LH12 (Gly-Leu-Leu-His-Leu-Leu-His-His-Leu-Leu-His-His-NH2) was designed utilizing the pH-sensitivity of histidine. Synthesized by Ontores Biotechnologies (China).
Experimental observations
LH12 displayed stronger antibacterial activity against S. mutans at pH 5.5 with MICs ranging from 12.00 μg/mL to 64.00 μg/mL. Figure 2d.
LH12 displayed stronger antibacterial activity against S. mutans at pH 5.5 with MBCs ranging from 12.00 μg/mL to 64.00 μg/mL. Figure 2d.
MICs at pH 7.2 ranging from 21.33 μg/mL to more than 128.00 μg/mL. Figure 2d.
MBCs at pH 7.2 ranging from 21.33 μg/mL to more than 128.00 μg/mL. Figure 2d.
LH12 displayed stronger antibacterial activity against E. coli at pH 5.5 with MICs ranging from 12.00 μg/mL to 64.00 μg/mL. Figure 2d.
LH12 displayed stronger antibacterial activity against E. coli at pH 5.5 with MBCs ranging from 12.00 μg/mL to 64.00 μg/mL. Figure 2d.
MICs at pH 7.2 ranging from 21.33 μg/mL to more than 128.00 μg/mL. Figure 2d.
MBCs at pH 7.2 ranging from 21.33 μg/mL to more than 128.00 μg/mL. Figure 2d.
LH12 displayed stronger antibacterial activity against S. aureus at pH 5.5 with MICs ranging from 12.00 μg/mL to 64.00 μg/mL. Figure 2d.
LH12 displayed stronger antibacterial activity against S. aureus at pH 5.5 with MBCs ranging from 12.00 μg/mL to 64.00 μg/mL. Figure 2d.
MICs at pH 7.2 ranging from 21.33 μg/mL to more than 128.00 μg/mL. Figure 2d.
MBCs at pH 7.2 ranging from 21.33 μg/mL to more than 128.00 μg/mL. Figure 2d.
The MICs of LH12 against S. mutans were from 8.00 μg/mL to 16.00 μg/mL. Figure 4a.
The MBCs were from 16.00 μg/mL to 32.00 μg/mL. Figure 4a.
The MICs of LH12 against A. viscosus were from 8.00 μg/mL to 16.00 μg/mL. Figure 4a.
The MBCs were from 16.00 μg/mL to 32.00 μg/mL. Figure 4a.
The MICs of LH12 against A. naeslundii were from 8.00 μg/mL to 16.00 μg/mL. Figure 4a.
The MBCs were from 16.00 μg/mL to 32.00 μg/mL. Figure 4a.
The MICs of LH12 against L. casei were from 8.00 μg/mL to 16.00 μg/mL. Figure 4a.
The MBCs were from 16.00 μg/mL to 32.00 μg/mL. Figure 4a.
The MICs of LH12 against L. fermentum were from 8.00 μg/mL to 16.00 μg/mL. Figure 4a.
The MBCs were from 16.00 μg/mL to 32.00 μg/mL. Figure 4a.
The MIC of LH12 against S. salivarius was 48.00 μg/mL. Figure 4a.
The MBC was 64.00 μg/mL. Figure 4a.
The MICs and MBCs of LH12 against S. sanguinis were no less than 128.00 μg/mL. Figure 4a.
The MICs and MBCs of LH12 against S. sanguinis were no less than 128.00 μg/mL. Figure 4a.
The MICs and MBCs of LH12 against S. gordonii were no less than 128.00 μg/mL. Figure 4a.
The MICs and MBCs of LH12 against S. gordonii were no less than 128.00 μg/mL. Figure 4a.
The MICs and MBCs of LH12 against S. mitis were no less than 128.00 μg/mL. Figure 4a.
The MICs and MBCs of LH12 against S. mitis were no less than 128.00 μg/mL. Figure 4a.
Only at a high concentration of 128 μg/mL would LH12 show slight cytotoxicity on HGECs with an inhibition ratio around 9.64% but without a significant reduction of the OD450 value after 45 min treatment. Figure 3a.
LH12 showed no hemolytic toxicity below 64 μg/mL and exhibited an increase of hemolysis ratio to 17.15% at 128 μg/mL. Figure 3c.
LH12 showed no hemolytic toxicity below 64 μg/mL. Figure 3c.
8 μg/mL LH12 could reduce 84.04% of biofilm mass. Figure 6a.
16 μg/mL and 32 μg/mL LH12 totally inhibited the biofilm formation. Figure 6a.
32 μg/mL LH12 reduced the viable S. mutans in the preformed biofilms. Figure 6e.
32 μg/mL LH12 reduced the biofilm thickness to a half of that in the control group. Figure 6f.
16 μg/mL and 32 μg/mL LH12 could decrease the lactic acid production of the preformed biofilms. Figure 6c.
16 μg/mL and 32 μg/mL LH12 could decrease the water-insoluble EPS synthesis of the preformed biofilms. Figure 6d.
LH12 could inhibit the formation of the dual-species biofilm. Figure 7a.
LH12 could reduce its strength to make it easier to remove. Figure 7b.
The short-term treatment of LH12 reduced the lactic acid production of the dual-species biofilm. Figure 7d.
The short-term treatment of LH12 reduced the water-insoluble EPS synthesis of the dual-species biofilm. Figure 7e.
Local peptide labels such as P1, PEP1, or peptide 1 are grouped only within this paper and are not assumed to represent the same molecule across publications.