1,4‐Dihydroxy‐2‐naphthoic acid from Propionibacterium freudenreichii reduces inflammation in interleukin‐10‐deficient mice with colitis by suppressing macrophage‐derived proinflammatory cytokines

Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society

关键词: inflammatory bowel diseases;    gut immunity;    beneficial bacteria;   

DOI  :  10.1189/jlb.0212104

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

Theanti‐inflammatorymechanismofprebioticshasrecentlybeenshowntohaveanimpactonthehostimmunesystem.DHNAfromPropionibacteriumfreudenreichiiisknowntopromotetheproliferationofBifidobacteriumandcanamelioratecolitis,althoughitsmodeofactionremainsunknown.Inthisstudy,weinvestigatedwhetherDHNAattenuatesinflammationinpiroxicam‐treatedIL‐10−/−mice,particularlyfocusingonthechangesofthehostimmunemechanism.DHNAwasadministeredtoIL‐10−/−micewithcolitis,andtheexpressionofadhesionmoleculesandmRNAlevelsofproinflammatorycytokinesweredetermined.DHNApretreatmentattenuatedthepiroxicam‐inducedhistologicalchanges.TheincreasedF4/80‐positivecellinfiltrationandVCAM‐1expressionweredecreasedbyDHNAadministration.TheincreasedmRNAlevelsofproinflammatorycytokineswerealsosuppressedbyDHNA.Ininvitroexperiments,increasedmRNAlevelsofproinflammatorycytokinesafterendotoxinexposureweredecreasedsignificantlybyDHNApretreatmentinRAW264.7,amacrophagecellline,andIL‐10−/−miceBMMs,whereastheexpressionofVCAM‐1inbEnd.3cells,aendothelialcellline,wasnotaffected.Takentogether,thesefindingssuggestthatadministrationofDHNAisusefulforthetreatmentofcolitisinpiroxicam‐treatedIL‐10−/−miceandthatattenuationofcolitisbyDHNAmaypartlybearesultofitsdirectactiononintestinalmacrophagestoinhibitproinflammatorycytokineproduction...

【 授权许可】

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