The global stress response regulator oxyS in an adherent-invasive Escherichia coli strain attenuates experimental colitis

Crohn’s disease and ulcerative colitis in humans and experimental immune-mediated colitis in mice are likely due in part to overactive immune responses to resident intestinal bacteria, including certain strains of adherent-invasive Escherichia coli (E. coli) such as E. coli NC101. We have previously...

Full description

Saved in:
Bibliographic Details
Main Authors: Diana Arsene, Sandrine Y. Tchaptchet, Jonathan J. Hansen
Format: Article
Language:English
Published: Taylor & Francis Group 2025-12-01
Series:Gut Microbes
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/19490976.2025.2473518
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849687584938131456
author Diana Arsene
Sandrine Y. Tchaptchet
Jonathan J. Hansen
author_facet Diana Arsene
Sandrine Y. Tchaptchet
Jonathan J. Hansen
author_sort Diana Arsene
collection DOAJ
description Crohn’s disease and ulcerative colitis in humans and experimental immune-mediated colitis in mice are likely due in part to overactive immune responses to resident intestinal bacteria, including certain strains of adherent-invasive Escherichia coli (E. coli) such as E. coli NC101. We have previously shown that specific E. coli NC101 stress responses are upregulated during experimental colitis and attenuate inflammation. However, the roles of broader stress response pathways in E. coli NC101 during experimental colitis are unknown. We hypothesize that the global stress response regulator in E. coli, oxyS, also reduces experimental colitis. We show that intestinal E. coli NC101 upregulate oxyS expression during colitis in monocolonized interleukin-10 deficient mice. Furthermore, we demonstrate that oxyS-sufficient E. coli NC101 have decreased motility and biofilm formation in vitro and attenuated intestinal translocation and colitogenic potential in vivo compared with oxyS-deficient E. coli. These data suggest that activation of a generalized E. coli stress response, oxyS, reduces experimental colitis and may be a potential therapeutic target.
format Article
id doaj-art-32701730a7904f579d972e992eca2eca
institution DOAJ
issn 1949-0976
1949-0984
language English
publishDate 2025-12-01
publisher Taylor & Francis Group
record_format Article
series Gut Microbes
spelling doaj-art-32701730a7904f579d972e992eca2eca2025-08-20T03:22:18ZengTaylor & Francis GroupGut Microbes1949-09761949-09842025-12-0117110.1080/19490976.2025.2473518The global stress response regulator oxyS in an adherent-invasive Escherichia coli strain attenuates experimental colitisDiana Arsene0Sandrine Y. Tchaptchet1Jonathan J. Hansen2Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC, USACenter for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC, USACenter for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC, USACrohn’s disease and ulcerative colitis in humans and experimental immune-mediated colitis in mice are likely due in part to overactive immune responses to resident intestinal bacteria, including certain strains of adherent-invasive Escherichia coli (E. coli) such as E. coli NC101. We have previously shown that specific E. coli NC101 stress responses are upregulated during experimental colitis and attenuate inflammation. However, the roles of broader stress response pathways in E. coli NC101 during experimental colitis are unknown. We hypothesize that the global stress response regulator in E. coli, oxyS, also reduces experimental colitis. We show that intestinal E. coli NC101 upregulate oxyS expression during colitis in monocolonized interleukin-10 deficient mice. Furthermore, we demonstrate that oxyS-sufficient E. coli NC101 have decreased motility and biofilm formation in vitro and attenuated intestinal translocation and colitogenic potential in vivo compared with oxyS-deficient E. coli. These data suggest that activation of a generalized E. coli stress response, oxyS, reduces experimental colitis and may be a potential therapeutic target.https://www.tandfonline.com/doi/10.1080/19490976.2025.2473518Stress responseinterleukin-10flagellummotilitytranslocation
spellingShingle Diana Arsene
Sandrine Y. Tchaptchet
Jonathan J. Hansen
The global stress response regulator oxyS in an adherent-invasive Escherichia coli strain attenuates experimental colitis
Gut Microbes
Stress response
interleukin-10
flagellum
motility
translocation
title The global stress response regulator oxyS in an adherent-invasive Escherichia coli strain attenuates experimental colitis
title_full The global stress response regulator oxyS in an adherent-invasive Escherichia coli strain attenuates experimental colitis
title_fullStr The global stress response regulator oxyS in an adherent-invasive Escherichia coli strain attenuates experimental colitis
title_full_unstemmed The global stress response regulator oxyS in an adherent-invasive Escherichia coli strain attenuates experimental colitis
title_short The global stress response regulator oxyS in an adherent-invasive Escherichia coli strain attenuates experimental colitis
title_sort global stress response regulator oxys in an adherent invasive escherichia coli strain attenuates experimental colitis
topic Stress response
interleukin-10
flagellum
motility
translocation
url https://www.tandfonline.com/doi/10.1080/19490976.2025.2473518
work_keys_str_mv AT dianaarsene theglobalstressresponseregulatoroxysinanadherentinvasiveescherichiacolistrainattenuatesexperimentalcolitis
AT sandrineytchaptchet theglobalstressresponseregulatoroxysinanadherentinvasiveescherichiacolistrainattenuatesexperimentalcolitis
AT jonathanjhansen theglobalstressresponseregulatoroxysinanadherentinvasiveescherichiacolistrainattenuatesexperimentalcolitis
AT dianaarsene globalstressresponseregulatoroxysinanadherentinvasiveescherichiacolistrainattenuatesexperimentalcolitis
AT sandrineytchaptchet globalstressresponseregulatoroxysinanadherentinvasiveescherichiacolistrainattenuatesexperimentalcolitis
AT jonathanjhansen globalstressresponseregulatoroxysinanadherentinvasiveescherichiacolistrainattenuatesexperimentalcolitis