Exploring the biological impact of bacteria-derived indole compounds on human cell health: Cytotoxicity and cell proliferation across six cell lines.
Janiga-MacNelly A., Vrazel M., Roat AE., Fernandez-Luna MT., Lavado R.
Laboratory Study, published in Toxicol Rep (2024) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Toxicol Rep (2024)
- Country
- Ireland
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 39844884
- PMCID
- PMC11750580
- DOI
- 10.1016/j.toxrep.2024.101883
- Citations
- 4
Abstract (original English)
Over the past two decades, research has increasingly focused on the interactions between diet, gut microbiota, and host organisms. Recent evidence suggests that tryptophan, an essential amino acid, can be metabolized by gut microbiota into indoles, which have significant biological effects. However, most research is limited to indole and its liver metabolite, indoxyl sulfate. This study examines the cytotoxic effects of five indole derivatives - indole-3-carboxylic acid (I3CA), indole-3-aldehyde (I3A), indole-3-acetic acid (IAA), indole-3-propionic acid (IPA), and 3-methylindole (skatole, 3-MI) - on six human cell lines: adipose-derived mesenchymal stem cells (MSC), hepatocellular carcinoma (HepG2), liver progenitor cells (HepaRG), colorectal carcinoma cells (Caco-2), breast cancer cells (T47D), and lung fibroblast (MRC-5). Results show no sensitivity to indole itself across cell lines. MRC-5 was sensitive to all other compounds (EC50 0.52-49.8 µM). MSCs responded to IPA, I3CA, I3A, and 3-MI (EC50 0.33-1.87 µM), while HepaRG cells were affected by IAA, I3CA, I3A, and 3-MI (EC50 1.98-66.4 µM). T47D cells were sensitive to IPA and IAA, and Caco-2 cells only to IAA (EC50 2.02, 1.68, 0.52 µM, respectively). HepG2 cells showed no change in viability. AhR activation in HepG2-AhR-Lucia cells was triggered by all derivatives, particularly I3A, IPA, and I3CA. Growth experiments revealed
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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