In Vitro Effects of Live and Heat-Inactivated Bifidobacterium animalis Subsp. Lactis, BB-12 and Lactobacillus rhamnosus GG on Caco-2 Cells

被引:23
作者
Castro-Herrera, Vivian M. [1 ]
Rasmussen, Christine [2 ]
Wellejus, Anja [2 ]
Miles, Elizabeth A. [1 ]
Calder, Philip C. [1 ,3 ,4 ]
机构
[1] Univ Southampton, Sch Human Dev & Hlth, Fac Med, Southampton SO16 6YD, Hants, England
[2] Chr Hansen AS, DK-2970 Horsholm, Denmark
[3] Univ Hosp Southampton NHS Fdn Trust, NIHR Southampton Biomed Res Ctr, Southampton SO16 6YD, Hants, England
[4] Univ Southampton, Southampton SO16 6YD, Hants, England
关键词
probiotic; gut epithelium; inflammation; B. animalis subsp. Lactis; BB-12; L. rhamnosus GG; heat-inactivation; INFLAMMASOME ACTIVATION; GROWTH-FACTOR; PROBIOTICS; INTERLEUKIN-6; EXPRESSION; ADHESION; MECHANISMS; PREVENTION; MEMBRANE; EFFICACY;
D O I
10.3390/nu12061719
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Probiotic-host interaction can be cell-to-cell or through metabolite production. Dead (inactive) organisms could interact with the host, leading to local effects and possible health benefits. This research examined the effects of live and heat-inactivatedBifidobacterium animalissubsp.lactis, BB-12 (BB-12) andLactobacillus rhamnosus GG(LGG) on cultured Caco-2 cells focusing on epithelial integrity and production of inflammatory mediators. Live organisms increased transepithelial electrical resistance (TEER), a barrier-integrity marker, with LGG having a greater effect than BB-12. When mildly heat-treated, both organisms had a more modest effect on TEER than when alive. When they were heat-inactivated, both organisms had only a limited effect on TEER. Neither live nor heat-inactivated organisms affected production of six inflammatory mediators produced by Caco-2 cells compared to control conditions. Pre-treatment with heat-inactivated LGG or BB-12 did not alter the decline in TEER caused by exposure to an inflammatory cocktail of cytokines. However, pre-treatment of Caco-2 cells with heat-inactivated organisms alone or their combination decreased the production of interleukin (IL)-6, IL-18, and vascular endothelial growth factor. To conclude, while the live organisms improve the epithelial barrier using this model, neither live nor heat-inactivated organisms directly elicit an inflammatory response by the epithelium. Pre-treatment with heat-inactivated BB-12 or LGG can reduce some components of the response induced by an inflammatory stimulus.
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页数:15
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