Polypeptides Isolated from <i>Lactococcus lactis</i> Alleviates Lipopolysaccharide (LPS)-Induced Inflammation in <i>Ctenopharyngodon idella</i>
The main purpose of the present study was to evaluate the anti-inflammatory activity of <i>Lactococcus lactis</i> BL52 and isolate active substances responsible for anti-inflammatory activity. Head-kidney (HK) macrophages were used for in vitro bioassay-guided isolation, and the structur...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2022-06-01
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| Series: | International Journal of Molecular Sciences |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1422-0067/23/12/6733 |
| Summary: | The main purpose of the present study was to evaluate the anti-inflammatory activity of <i>Lactococcus lactis</i> BL52 and isolate active substances responsible for anti-inflammatory activity. Head-kidney (HK) macrophages were used for in vitro bioassay-guided isolation, and the structure of the two peptides was identified by mass spectrometry analysis. Lipopolysaccharide (LPS)-induced inflammatory responses in <i>Ctenopharyngodon idella</i> were also examined to evaluate the in vivo anti-inflammatory activity of active substances. Two active peptides were isolated by HPLC from <i>L</i><i>. lactis</i> BL52, and an in vitro anti-inflammatory assay demonstrated that peptide ALBL1 and ALBL2 dose-dependently inhibited LPS-induced inflammatory cytokines TNF-α, IL-6, and IL-1β and inflammatory factors NO and PGE 2 production in macrophages (<i>p</i> < 0.05). After being treated with 20 mg/Kg peptide ALBL1 and ALBL2, the expression levels of TNF-α, IL-6, IL-1β, NO, and PGE 2 were significantly inhibited (<i>p</i> < 0.05). Results from the in vivo test showed that when the concentration of peptide ALBL1 and ALBL2 reached 30 mg/Kg, the LPS-induced upregulations of TNF-α, IL-6, IL-1β, NO, and PGE 2 were prevented. In addition, peptide ALBL1 and ALBL2 blocked the expression of Toll-like receptor 2 (TLR2) and then suppressed the phosphorylation of nuclear transcription factor-kappa B (NF-κB) p65 and degradation inhibitor of IκBα. Moreover, <i>C. idella</i> treated with peptide ALBL1 and ALBL2 can relieve pathological inflammatory responses caused by LPS. These results suggest that the anti-inflammatory properties of peptide ALBL1 and ALBL2 might be a result from the inhibition of IL-6, IL-1β, and TNF-α expressions through the downregulation of Toll2/NF-κB signaling pathways. |
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| ISSN: | 1661-6596 1422-0067 |