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Benef Microbes. 2017 Apr 26;8(2):257-269. doi: 10.3920/BM2016.0119. Epub 2017 Apr 14.

Bifidobacterium animalis subsp. lactis 420 mitigates the pathological impact of myocardial infarction in the mouse.

Author information

1
1 Department of Physiology, Sarver Molecular Cardiovascular Research Program, University of Arizona, Tucson, AZ 85724, USA.
2
4 Department of Neurobiology, University of Arizona, Tucson, AZ 85721, USA.
3
5 Arizona Center for Aging, University of Arizona, Tucson, AZ 85719, USA.
4
6 Department of Medicine, University of Arizona, Tucson, AZ 85721, USA.
5
2 DuPont Nutrition and Health, Active Nutrition, Sokeritehtaantie 20, 02460 Kantvik, Finland.
6
3 Department of Immunobiology, University of Arizona, Tucson, AZ 85724, USA.
7
7 Department Surgery, University of Arizona, Tucson, AZ 85721, USA.

Abstract

There is a growing appreciation that our microbial environment in the gut plays a critical role in the maintenance of health and the pathogenesis of disease. Probiotic, beneficial gut microbes, administration can directly attenuate cardiac injury and post-myocardial infarction (MI) remodelling, yet the mechanisms of cardioprotection are unknown. We hypothesised that administration of Bifidobacterium animalis subsp. lactis 420 (B420), a probiotic with known anti-inflammatory properties, to mice will mitigate the pathological impact of MI, and that anti-inflammatory T regulatory (Treg) immune cells are necessary to impart protection against MI as a result of B420 administration. Wild-type male mice were administered B420, saline or Lactobacillus salivarius 33 (Ls-33) by gavage daily for 14 or 35 days, and underwent ischemia/reperfusion (I/R). Pretreatment with B420 for 10 or 28 days attenuated cardiac injury from I/R and reduced levels of inflammatory markers. Depletion of Treg cells by administration of anti-CD25 monoclonal antibodies eliminated B420-mediated cardio-protection. Further cytokine analysis revealed a shift from a pro-inflammatory to an anti-inflammatory environment in the probiotic treated post-MI hearts compared to controls. To summarise, B420 administration mitigates the pathological impact of MI. Next, we show that Treg immune cells are necessary to mediate B420-mediated protection against MI. Finally, we identify putative cellular, epigenetic and/or post-translational mechanisms of B420-mediated protection against MI.

KEYWORDS:

B. animalis ssp. lactis; cardiovascular disease; inflammation; probiotics; regulatory T cells

PMID:
28409534
PMCID:
PMC5815367
DOI:
10.3920/BM2016.0119
[Indexed for MEDLINE]
Free PMC Article

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