Mechanism of regulation of plasmic reticulum stress and prevention of inflammation in combination with Ligilactobacillus salivarius B112 from Min pigs
The aim of this study was to investigate the mechanism by which Ligilactobacillus sali-varius of porcine origin alleviates LPS-induced inflammation in porcine small intestine epithelial cells(IPEC-J2)by regulating endoplasmic reticulum stress.In this study,a strain B112 was isolated from the intestinal tract of Min pigs with good disease resistance and cold tolerance and identified as Ligilactobacillus salivarius.The diameter of inhibition zone of Ligilactobacillus salivarius from this strain and Ternary hybrid pig against Escherichia coli,Salmonella and Staphylococcus aureus was detected by single plate punching method.In addition,in vi tro cell model construction method was used to pretreat IPEC-J2 with Ligilactobacillus salivarius B1 12,and then stimulate IPEC-J2 with LPS to sim-ulate intestinal inflammation,and real-time fluorescence quantitative PCR was used to detect the changes of inflammatory factors and endoplasmic reticulum stress related factors.The results of bac-teriostatic test showed that Ligilactobacillus salivarius B112 from Min pigs had bacteriostatic effect on all three pathogenic bacteria,and had better bacteriostatic effect on Staphylococcus aureus and Escherichia coli,while Ligilactobacillus salivarius JCM1231 from Ternary hybrid pig had no bacterio-static effect on Staphylococcus aureus,but its bacteriostatic effect on Salmonella was stronger than that of Bacillus from porcine.The results of in vitro anti-inflammatory tests showed that Ligilacto-bacillus salivarius B112 from Min pigs could decrease the mRNA expression of LPS induced inflammatory factors such as IL-6 and ER stress factors such as GRP78.In summary,Ligilactobacillus salivarius B112 isolated from the intestinal tract of Min pigs can inhibit the growth and reproduction of Escherichia coli,Salmonella and Staphylococcus aureus,and can regulate endoplasmic reticulum stress to relieve the inflammation caused by IPEC-J2 stimulated by LPS.It is expected to provide theoretical basis and technical reference for further development and application of Ligilactobacillus salivarius in resisting intestinal inflammation of weaned piglets.
Min pigsLigilactobacillus salivariusisolation and identificationendoplasmic reticulum stressintestinal inflammation
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