Microbial lysate upregulates host oxytocin
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Author(s)
Poutahidis, Theofilos
DiBenedictis, Brett T.
Levkovich, Tatiana
Ibrahim, Yassin
Shikhman, Lana
Cheung, Harry K.
Hardas, Alexandros
Ricciardi, Catherine E.
Kolandaivelu, Kumaran
Veenema, Alexa H.
Date Issued
November 2016
Journal
Brain, Behavior, and Immunity
Publisher
Elsevier
Citation
Varian, Bernard J. et al. “Microbial Lysate Upregulates Host Oxytocin.” Brain, Behavior, and Immunity 61 (March 2017): 36–49 © 2016 The Authors
Version
Author's final manuscript
Abstract
Neuropeptide hormone oxytocin has roles in social bonding, energy metabolism, and wound healing contributing to good physical, mental and social health. It was previously shown that feeding of a human commensal microbe Lactobacillus reuteri (L. reuteri) is sufficient to up-regulate endogenous oxytocin levels and improve wound healing capacity in mice. Here we show that oral L. reuteri-induced skin wound repair benefits extend to human subjects. Further, dietary supplementation with a sterile lysate of this microbe alone is sufficient to boost systemic oxytocin levels and improve wound repair capacity. Oxytocin-producing cells were found to be increased in the caudal paraventricular nucleus [PVN] of the hypothalamus after feeding of a sterile lysed preparation of L. reuteri, coincident with lowered blood levels of stress hormone corticosterone and more rapid epidermal closure, in mouse models. We conclude that microbe viability is not essential for regulating host oxytocin levels. The results suggest that a peptide or metabolite produced by bacteria may modulate host oxytocin secretion for potential public or personalized health goals. Keywords:
Bacteria; Postbiotic; Stress; Corticosterone; Thymus; Wound healing
MIT Department
Massachusetts Institute of Technology. Department of Biological Engineering
Massachusetts Institute of Technology. Department of Civil and Environmental Engineering
Massachusetts Institute of Technology. Division of Comparative Medicine
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Creative Commons Attribution-NonCommercial-NoDerivs License
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DOI of Published Version
https://doi.org/10.1016/J.BBI.2016.11.002
