PMID- 35743169
OWN - NLM
STAT- MEDLINE
DCOM- 20220627
LR  - 20230308
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 23
IP  - 12
DP  - 2022 Jun 16
TI  - Polypeptides Isolated from Lactococcus lactis Alleviates Lipopolysaccharide 
      (LPS)-Induced Inflammation in Ctenopharyngodon idella.
LID - 10.3390/ijms23126733 [doi]
LID - 6733
AB  - The main purpose of the present study was to evaluate the anti-inflammatory 
      activity of Lactococcus lactis 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 Ctenopharyngodon idella were also examined to evaluate the in vivo 
      anti-inflammatory activity of active substances. Two active peptides were 
      isolated by HPLC from L. lactis BL52, and an in vitro anti-inflammatory assay 
      demonstrated that peptide ALBL1 and ALBL2 dose-dependently inhibited LPS-induced 
      inflammatory cytokines TNF-alpha, IL-6, and IL-1beta and inflammatory factors NO and PGE 
      2 production in macrophages (p < 0.05). After being treated with 20 mg/Kg peptide 
      ALBL1 and ALBL2, the expression levels of TNF-alpha, IL-6, IL-1beta, NO, and PGE 2 were 
      significantly inhibited (p < 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-alpha, IL-6, IL-1beta, 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-kappaB) p65 and degradation inhibitor of IkappaBalpha. Moreover, C. idella 
      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-1beta, and TNF-alpha expressions through the downregulation of Toll2/NF-kappaB 
      signaling pathways.
FAU - Li, Pei
AU  - Li P
AD  - College of Life Science and Technology, Guangxi University, Nanning 530004, 
      China.
AD  - Institute for Fishery Sciences, Guangxi University, Nanning 530004, China.
AD  - Agricultural Products Processing Research Institute, Chinese Academy of Tropical 
      Agricultural Sciences, Zhanjiang 524000, China.
FAU - Xu, Youqing
AU  - Xu Y
AD  - Institute for Fishery Sciences, Guangxi University, Nanning 530004, China.
FAU - Cao, Yupo
AU  - Cao Y
AD  - Agricultural Products Processing Research Institute, Chinese Academy of Tropical 
      Agricultural Sciences, Zhanjiang 524000, China.
FAU - Ding, Zhaokun
AU  - Ding Z
AD  - Institute for Fishery Sciences, Guangxi University, Nanning 530004, China.
LA  - eng
GR  - 1630122017020/Central Public-interest Scientific Institution Basal Research Fund 
      for Chinese Academy of Tropical Agricultural Sciences/
PT  - Journal Article
DEP - 20220616
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/therapeutic use
MH  - *Carps/metabolism
MH  - Dinoprostone/metabolism
MH  - Inflammation/chemically induced/drug therapy/metabolism
MH  - Interleukin-6
MH  - *Lactococcus lactis/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - NF-kappa B/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC9224536
OTO - NOTNLM
OT  - Ctenopharyngodon idella
OT  - Lactococcus lactis
OT  - anti-inflammatory
OT  - bioassay-guided isolation
OT  - lipopolysaccharide
OT  - polypeptide
COIS- The authors declare no conflict of interest.
EDAT- 2022/06/25 06:00
MHDA- 2022/06/28 06:00
PMCR- 2022/06/16
CRDT- 2022/06/24 01:22
PHST- 2022/04/14 00:00 [received]
PHST- 2022/05/22 00:00 [revised]
PHST- 2022/06/07 00:00 [accepted]
PHST- 2022/06/24 01:22 [entrez]
PHST- 2022/06/25 06:00 [pubmed]
PHST- 2022/06/28 06:00 [medline]
PHST- 2022/06/16 00:00 [pmc-release]
AID - ijms23126733 [pii]
AID - ijms-23-06733 [pii]
AID - 10.3390/ijms23126733 [doi]
PST - epublish
SO  - Int J Mol Sci. 2022 Jun 16;23(12):6733. doi: 10.3390/ijms23126733.