The Yin and Yang of bile acid action on tight junctions in a model colonic epithelium
Open accessAbstract
Gastrointestinal epithelial barrier loss due to tight junction (TJ) dysfunction and bile acid-induced diarrhea are common in patients with inflammatory diseases. Although excess colonic bile acids are known to alter mucosal permeability, few studies have compared the effects of specific bile acids on TJ function. We report that the primary bile acid, chenodeoxycholic acid (CDCA), and its 7α-dehydroxylated derivative, lithocholic acid (LCA) have opposite effects on epithelial integrity in human colonic T84 cells. CDCA decreased transepithelial barrier resistance (pore) and increased paracellular 10 kDa dextran permeability (leak), effects that were enhanced by proinflammatory cytokines (PiC [ng/mL]: TNFα[10] + IL-1ß[10] + IFNγ[30]). CDCA reversed the cation selectivity of the monolayer and decreased intercellular adhesion. In contrast, LCA alone did not alter any of these parameters, but attenuated the effects of CDCA ± PiC on paracellular permeability. CDCA, but not PiC, decreased occludin and not claudin-2 protein expression; CDCA also decreased occludin localization. LCA ± CDCA had no effects on occludin or claudin expression/localization. While PiC and CDCA increased IL-8 production, LCA reduced both basal and PiC ± CDCA-induced IL-8 production. TNFα + IL1ß increased IFNγ, which was enhanced by CDCA and attenuated by LCA. CDCA±PiC increased production of reactive oxygen species (ROS) that was attenuated by LCA. Finally, scavenging ROS attenuated CDCA's leak, but not pore actions, and LCA enhanced this effect. Thus, in T84 cells, CDCA plays a role in the inflammatory response causing barrier dysfunction, while LCA restores barrier integrity. Understanding the interplay of LCA, CDCA, and PiC could lead to innovative therapeutic strategies for inflammatory and diarrheal diseases.
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Activation of TGR5 is generally associated with anti-inflammatory effects and protective features towards the intestinal epithelium.
“Activation of TGR5 has generally been associated with anti-inflammatory effects and protective features towards the intestinal epithelium (Sarathy et al., 2017;Ward et al., 2017).”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Sarathy et al., 2017
The Discussion says TGR5 activation in macrophages mediates expression of the pro-inflammatory cytokines IL-1β and TNF-α. It also says the reported effects of LCA in T84 epithelial cells are not mediated by TGR5. Thus, this paper does not associate TGR5 activation with the anti-inflammatory, epithelial-protective effects claimed. (LLM, conf=0.84)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredSome bile acid metabolites can both improve as well as exert negative effects on gut barrier tight junction function.
“Some bile acid metabolites can both improve as well as exert negative effects on gut barrier TJ function.104”
From Regulation of Intestinal Barrier Function by Microbial Metabolites (2021) · cites this paper as [104]
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Mulak, A. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210608 · Cited by 114 · see citing works
- Authors
- Sarathy, J., Detloff, S. J., Ao, M., Khan, N., French, S., Sirajuddin, H., Nair, T., & Rao, M. C.
- Affiliations
- Benedictine University (US)
- University of Illinois Chicago (US)
- Corresponding author
- Sarathy, Jayashree
- Rao, Mrinalini C.
- Venue
- Physiological Reports
- Publisher
- Wiley
- Published
- 2017-05
- Volume
- 5
- Issue
- 10
- Pages
- e13294-e13294
- ISSN
- 2051-817X (ISSN-L)
- PMC
- PMC5449568
- OpenAlex
- W2618166136
- Cited by
- 72
- References
- 94
- Citations by year
- 2026: 10 · 2025: 12 · 2024: 8 · 2023: 4 · 2022: 7 · 2021: 8 · 2020: 7 · 2019: 13 · 2018: 3
- FWCI
- 3.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Physiological Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- University of Illinois
- National Science Foundation (NSF‐MRI: DBI‐1427937)
- Topics
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Keywords
- bile acids, chenodeoxycholic acid, lithocholic acid, tight junctions, colonic epithelium, intestinal barrier dysfunction, paracellular permeability, inflammatory cytokines, occludin, claudin-2, interleukin-8, reactive oxygen species, T84 cells, inflammatory bowel disease
- MeSH terms
- Bile Acids and Salts, Cell Adhesion, Chenodeoxycholic Acid, Colon, Humans, Inflammation, Intestinal Mucosa, Lithocholic Acid, Permeability, Cytokines, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Tight Junctions, Cell Line, Tumor
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