Stress and antibiotics alter luminal and wall‐adhered microbiota and enhance the local expression of visceral sensory‐related systems in mice
Abstract
Background: Stress leads to altered gastrointestinal neuro‐immune responses. We characterized the interaction between stress and gut commensal microbiota and their role modulating colonic responses to stress, the induction of inflammation, the expression of sensory‐related markers, and visceral sensitivity. Methods: C57BL/6N female mice were treated (7 days, PO) with non‐absorbable‐broad spectrum antibiotics (bacitracin/neomycin, 0.4 mg per mouse per day). Simultaneously, mice were subjected to a 1 h per day (7 days) session of psychological stress (water avoidance stress, WAS). Luminal and wall‐adhered microbiota were characterized by fluorescent in situ hybridization. Cannabinoid receptors 1 and 2 (CB1/2), tryptophan hydroxylase 1 and 2 (TPH1/2), and inflammatory markers were quantified by reverse transcription–quantitative real‐time PCR (RT‐qPCR) and secretory‐IgA (s‐IgA) by ELISA. Visceral sensitivity was assessed after the intracolonic administration of capsaicin. Key Results: Antibiotics did not affect the defecatory and endocrine responses to stress. However, antibiotics diminished by 2.5‐folds total bacterial counts, induced a specific dysbiosis and favored bacterial wall adherence. Combining antibiotics and stress resulted in further reductions in bacterial counts and a dysbiosis, with enhanced bacterial wall adherence. Luminal s‐IgA levels increased in dysbiotic mice. Nevertheless, no alterations consistent with the induction of colonic inflammation were observed. Dysbiosis upregulated CB 2 expression and stress upregulated CB 2 and TPH 1 expression. Stress enhanced visceral pain‐related responses, an effect prevented by antibiotic treatment. Conclusions & Inferences: Manipulations of the commensal microbiota and the interaction host–microbiota are able to modulate the local expression of neuro–immune–endocrine systems within the colon, leading to a modulation of visceral sensitivity. These mechanisms might contribute to the pathogenic and protective roles of microbiota in gastrointestinal homeostasis.
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Gut microbiota may directly modulate several systems involved in visceral hypersensitivity.
“Recent data have shown that gut microbiota may directly modulate several systems involved in visceral hypersensitivity.”
From Gut microbiota role in irritable bowel syndrome: New therapeutic strategies (2016) · cites this paper as [116]
Several studies linking the gut microbiota with visceral sensitivity have shown that increments in the Lactobacilli family are associated to visceral analgesic-like states.
“Moreover, several studies linking the gut microbiota with visceral sensitivity, have shown that increments in the Lactobacilli family (during probiotic treatment or during states of dysbiosis) are associated to visceral analgesic-like states.18,19,21,33”
From Antibiotic-induced dysbiosis alters host-bacterial interactions and leads to colonic sensory and motor changes in mice (2015) · cites this paper as [19]
Specific alterations in the composition of the GCM modify the expression of the intestinal endocannabinoid system, affecting nociceptive responses in mice.
“For instance, we have recently shown that specific alterations in the composition of the GCM modify the expression of the intestinal endocannabinoid system, affecting nociceptive responses in mice.19”
From Antibiotic-induced dysbiosis alters host-bacterial interactions and leads to colonic sensory and motor changes in mice (2015) · cites this paper as [19]
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- Authors
- Aguilera, M., Vergara, P., & Martínez, V.
- Affiliations
- Universitat Autònoma de Barcelona (ES)
- Department of Cell Biology, Physiology and Immunology Universitat Autònoma de Barcelona Bellaterra Barcelona Spain
- Venue
- Neurogastroenterology & Motility
- Publisher
- Wiley
- Published
- 2013-05-27
- Volume
- 25
- Issue
- 8
- Pages
- e515-29
- ISSN
- 1350-1925 (ISSN-L)
- 1365-2982
- OpenAlex
- W2041215328
- Cited by
- 119
- References
- 67
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 5 · 2023: 11 · 2022: 13 · 2021: 15 · 2020: 7 · 2019: 6 · 2018: 13 · 2017: 8 · 2016: 15 · 2015: 7 · 2014: 9 · 2013: 4
- FWCI
- 5.22
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurogastroenterology & Motility (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
- Keywords
- psychological stress, gut microbiota, dysbiosis, antibiotic-induced dysbiosis, visceral sensitivity, visceral pain, gut-brain axis, cannabinoid receptors, CB2, tryptophan hydroxylase, secretory IgA, colonic inflammation, water avoidance stress, capsaicin
- MeSH terms
- Animals, Anti-Bacterial Agents, Colon, Female, Intestinal Mucosa, Mice, Inbred C57BL, Random Allocation, Stress, Psychological, Up-Regulation, Mice, Visceral Pain, Microbiota
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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