{"title":"Mannan rich fraction from yeast modulates inflammatory responses in intestinal cells (HT-29) exposed toEscherichia coli","authors":"N. Browne, A. Traynor, K. Horgan","doi":"10.1017/JAN.2019.5","DOIUrl":null,"url":null,"abstract":"Mannan from yeast has been demonstrated to limit infection in animals susceptible to gastrointestinal infection, including pigs, poultry and cows, by blocking the mechanism by which gram-negative bacteria adhere to and invade the intestines. EnterotoxigenicEscherichia coli(ETEC) cause post weaning diarrhoea (PWD) which results in poor weight gain and potential death at great economic cost to the farmer. A mannan rich fraction (MRF) was assessedin vitrofor its impact on ETEC infection of HT-29 intestinal cell line. Gene expression markers for inflammation (TNFαandIL-1β) and TLR4 (TICAM-1andLY96) associated recognition of bacteria were significantly elevated following exposure toE. colialone, but not in combination with MRF compared to the control. HT-29 cells exposed to MRF alone demonstrated significantly reduced expression of immune signalling genesIRAK1,IRF7andJUNwhen compared to the control. HT-29 cell protein abundance for TNFα and TLR4 associated proteins were significantly increased in response toE. coliexposure alone while no significant change was observed for MRF treatment withE. coliinfection.E. coliadhesion to HT-29 cells was significantly decreased with addition of MRF compared toE. coliinfection alone. The action of MRF demonstrated its potential capacity to limit infection on anin vitrolevel through blocking bacterial interaction with the intestines that leads to infection as marked by a reduction in proinflammatory responses. MRF on its own demonstrated potential anti-inflammatory effects on intestinal cells with the reduction of proinflammatory responses observed.","PeriodicalId":36124,"journal":{"name":"Journal of Applied Animal Nutrition","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/JAN.2019.5","citationCount":"3","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Applied Animal Nutrition","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1017/JAN.2019.5","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Agricultural and Biological Sciences","Score":null,"Total":0}
引用次数: 3
Abstract
Mannan from yeast has been demonstrated to limit infection in animals susceptible to gastrointestinal infection, including pigs, poultry and cows, by blocking the mechanism by which gram-negative bacteria adhere to and invade the intestines. EnterotoxigenicEscherichia coli(ETEC) cause post weaning diarrhoea (PWD) which results in poor weight gain and potential death at great economic cost to the farmer. A mannan rich fraction (MRF) was assessedin vitrofor its impact on ETEC infection of HT-29 intestinal cell line. Gene expression markers for inflammation (TNFαandIL-1β) and TLR4 (TICAM-1andLY96) associated recognition of bacteria were significantly elevated following exposure toE. colialone, but not in combination with MRF compared to the control. HT-29 cells exposed to MRF alone demonstrated significantly reduced expression of immune signalling genesIRAK1,IRF7andJUNwhen compared to the control. HT-29 cell protein abundance for TNFα and TLR4 associated proteins were significantly increased in response toE. coliexposure alone while no significant change was observed for MRF treatment withE. coliinfection.E. coliadhesion to HT-29 cells was significantly decreased with addition of MRF compared toE. coliinfection alone. The action of MRF demonstrated its potential capacity to limit infection on anin vitrolevel through blocking bacterial interaction with the intestines that leads to infection as marked by a reduction in proinflammatory responses. MRF on its own demonstrated potential anti-inflammatory effects on intestinal cells with the reduction of proinflammatory responses observed.