Individual differences in stress vulnerability: The role of gut pathobionts in stress-induced colitis
Name
Fox-Langgartner.pdf
Description
Accepted version
Size
636.95 KB
Format
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Checksum (MD5)
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Author(s)
Langgartner, Dominik
Peterlik, Daniel
Foertsch, Sandra
Füchsl, Andrea M.
Brokmann, Petra
Flor, Peter J.
Shen, Zeli
Fox, James G
Uschold-Schmidt, Nicole
Lowry, Christopher A.
Date Issued
December 2016
Journal
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Citation
Langgartner, Dominik et al. "Individual differences in stress vulnerability: The role of gut pathobionts in stress-induced colitis." Brain, Behavior, and Immunity 64 (August 2017): 23-32 © Elsevier
Version
Author's final manuscript
Abstract
Chronic subordinate colony housing (CSC), an established mouse model for chronic psychosocial stress, promotes a microbial signature of gut inflammation, characterized by expansion of Proteobacteria, specifically Helicobacter spp., in association with colitis development. However, whether the presence of Helicobacter spp. during CSC is critically required for colitis development is unknown. Notably, during previous CSC studies performed at Regensburg University (University 1), male specific-pathogen-free (SPF) CSC mice lived in continuous subordination to a physically present and Helicobacter spp.-positive resident. Therefore, it is likely that CSC mice were colonized, during the CSC procedure, with Helicobacter spp. originating from the dominant resident. In the present study we show that employing SPF CSC mice and Helicobacter spp.-free SPF residents at Ulm University (University 2), results in physiological responses that are typical of chronic psychosocial stress, including increased adrenal and decreased thymus weights, decreased adrenal in vitro adrenocorticotropic hormone (ACTH) responsiveness, and increased anxiety-related behavior. However, in contrast to previous studies that used Helicobacter spp.-positive resident mice, use of Helicobacter spp.-negative resident mice failed to induce spontaneous colitis in SPF CSC mice. Consistent with the hypothesis that the latter is due to a lack of Helicobacter spp. transmission from dominant residents to subordinate mice during the CSC procedure, colonization of SPF residents with Helicobacter typhlonius at University 2, prior to the start of the CSC model, rescued the colitis-inducing potential of CSC exposure. Furthermore, using SPF CSC mice and H. typhlonius-free SPF residents at University 1 prevented CSC-induced colitis. In summary, our data support the hypothesis that the presence or absence of exposure to certain pathobionts contributes to individual variability in susceptibility to stress-/trauma-associated pathologies and to reproducibility of stress-related outcomes between laboratories. Keywords: Chronic psychosocial stress; Chronic subordinate colony housing (CSC); Enterohepatic Helicobacter species (EHS); Inflammatory bowel disease (IBD); Microbiota; Colitis; Stress vulnerability; Stress resilience; Inflammation; Pathobionts
MIT Department
Massachusetts Institute of Technology. Division of Comparative Medicine
Massachusetts Institute of Technology. Department of Biological Engineering
Terms of Use
Creative Commons Attribution-NonCommercial-NoDerivs License
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DOI of Published Version
https://doi.org/10.1016/j.bbi.2016.12.019
