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

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-inactivated Bifidobacterium animalis subsp. lactis, BB-1...

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Autores principales: Castro-Herrera, Vivian M., Rasmussen, Christine, Wellejus, Anja, Miles, Elizabeth A., Calder, Philip C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7352502/
https://www.ncbi.nlm.nih.gov/pubmed/32521765
http://dx.doi.org/10.3390/nu12061719
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author Castro-Herrera, Vivian M.
Rasmussen, Christine
Wellejus, Anja
Miles, Elizabeth A.
Calder, Philip C.
author_facet Castro-Herrera, Vivian M.
Rasmussen, Christine
Wellejus, Anja
Miles, Elizabeth A.
Calder, Philip C.
author_sort Castro-Herrera, Vivian M.
collection PubMed
description 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-inactivated Bifidobacterium animalis subsp. lactis, BB-12 (BB-12) and Lactobacillus 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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spelling pubmed-73525022020-07-15 In Vitro Effects of Live and Heat-Inactivated Bifidobacterium animalis Subsp. Lactis, BB-12 and Lactobacillus rhamnosus GG on Caco-2 Cells Castro-Herrera, Vivian M. Rasmussen, Christine Wellejus, Anja Miles, Elizabeth A. Calder, Philip C. Nutrients Article 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-inactivated Bifidobacterium animalis subsp. lactis, BB-12 (BB-12) and Lactobacillus 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. MDPI 2020-06-08 /pmc/articles/PMC7352502/ /pubmed/32521765 http://dx.doi.org/10.3390/nu12061719 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Castro-Herrera, Vivian M.
Rasmussen, Christine
Wellejus, Anja
Miles, Elizabeth A.
Calder, Philip C.
In Vitro Effects of Live and Heat-Inactivated Bifidobacterium animalis Subsp. Lactis, BB-12 and Lactobacillus rhamnosus GG on Caco-2 Cells
title In Vitro Effects of Live and Heat-Inactivated Bifidobacterium animalis Subsp. Lactis, BB-12 and Lactobacillus rhamnosus GG on Caco-2 Cells
title_full In Vitro Effects of Live and Heat-Inactivated Bifidobacterium animalis Subsp. Lactis, BB-12 and Lactobacillus rhamnosus GG on Caco-2 Cells
title_fullStr In Vitro Effects of Live and Heat-Inactivated Bifidobacterium animalis Subsp. Lactis, BB-12 and Lactobacillus rhamnosus GG on Caco-2 Cells
title_full_unstemmed In Vitro Effects of Live and Heat-Inactivated Bifidobacterium animalis Subsp. Lactis, BB-12 and Lactobacillus rhamnosus GG on Caco-2 Cells
title_short In Vitro Effects of Live and Heat-Inactivated Bifidobacterium animalis Subsp. Lactis, BB-12 and Lactobacillus rhamnosus GG on Caco-2 Cells
title_sort in vitro effects of live and heat-inactivated bifidobacterium animalis subsp. lactis, bb-12 and lactobacillus rhamnosus gg on caco-2 cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7352502/
https://www.ncbi.nlm.nih.gov/pubmed/32521765
http://dx.doi.org/10.3390/nu12061719
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