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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

In vitro effects of live and heat-inactivated Bifidobacterium animalis subsp. lactis, BB-12 and Lactobacillus rhamnosus GG on Caco-2 cells
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-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.
B. Animalis subsp, BB-12, Gut epithelium, Heat-inactivation, Inflammation, L. Rhamnosus GG, Lactis, Probiotic
2072-6643
Castro Herrera, Vivian Maritza
ee06e5c1-815f-497f-9c67-47ead3772704
Rasmussen, Christine
5c7270f0-453c-4622-98a7-51d006b52d53
Wellejus, Anja
b03ecf04-d89c-496b-a29c-48f7df4c86b3
Miles, Elizabeth
20332899-ecdb-4214-95bc-922dde36d416
Calder, Philip
1797e54f-378e-4dcb-80a4-3e30018f07a6
Castro Herrera, Vivian Maritza
ee06e5c1-815f-497f-9c67-47ead3772704
Rasmussen, Christine
5c7270f0-453c-4622-98a7-51d006b52d53
Wellejus, Anja
b03ecf04-d89c-496b-a29c-48f7df4c86b3
Miles, Elizabeth
20332899-ecdb-4214-95bc-922dde36d416
Calder, Philip
1797e54f-378e-4dcb-80a4-3e30018f07a6

Castro Herrera, Vivian Maritza, Rasmussen, Christine, Wellejus, Anja, Miles, Elizabeth and Calder, Philip (2020) In vitro effects of live and heat-inactivated Bifidobacterium animalis subsp. lactis, BB-12 and Lactobacillus rhamnosus GG on Caco-2 cells. Nutrients, 12 (6), [1719]. (doi:10.3390/nu12061719).

Record type: Article

Abstract

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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Castro-Herrera et al_Accepted Version_Nutrients - Accepted Manuscript
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Accepted/In Press date: 5 June 2020
e-pub ahead of print date: 8 June 2020
Keywords: B. Animalis subsp, BB-12, Gut epithelium, Heat-inactivation, Inflammation, L. Rhamnosus GG, Lactis, Probiotic

Identifiers

Local EPrints ID: 441450
URI: http://eprints.soton.ac.uk/id/eprint/441450
ISSN: 2072-6643
PURE UUID: ba438bed-ee1d-42dd-ae69-cef7cda2bef7
ORCID for Elizabeth Miles: ORCID iD orcid.org/0000-0002-8643-0655
ORCID for Philip Calder: ORCID iD orcid.org/0000-0002-6038-710X

Catalogue record

Date deposited: 12 Jun 2020 16:40
Last modified: 26 Nov 2021 02:38

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Contributors

Author: Vivian Maritza Castro Herrera
Author: Christine Rasmussen
Author: Anja Wellejus
Author: Elizabeth Miles ORCID iD
Author: Philip Calder ORCID iD

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