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Melatonin Mitigates Oxazolone-Induced Colitis in Microbiota-Dependent Manner
Zi-Xiao Zhao1,2, Xi Yuan3, Yan-Yan Cui3
1Department of Gastroenterology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Frontiers in Immunology
|February 4, 2022
Summary
Melatonin alleviates oxazolone-induced colitis by modulating gut microbiota and suppressing type 2 immunity. This suggests melatonin
Area of Science:
- Immunology
- Gastroenterology
- Microbiology
Background:
- Elevated type 2 cytokines are observed in active ulcerative colitis (UC).
- Melatonin's efficacy in some colitis models is known, but its role in type 2 immunity-driven colitis is unclear.
- A negative correlation between melatonin levels and UC severity was observed.
Purpose of the Study:
- To investigate melatonin's effects in oxazolone (Oxa)-induced colitis, a model of type 2 immunity-driven inflammation.
- To elucidate the mechanisms underlying melatonin's protective actions, focusing on immune response and gut microbiota.
Main Methods:
- Oxa-induced colitis model in mice.
- Melatonin administration and assessment of clinical and histological parameters.
- Analysis of immune cell infiltration, intestinal permeability markers (ZO-1, occludin).
- 16S rRNA sequencing for gut microbiota profiling.
- Fecal microbiota transplantation (FMT) experiments.
Main Results:
- Melatonin treatment significantly reduced body weight loss, colon shortening, and neutrophil infiltration in Oxa-induced colitis.
- Melatonin suppressed the type 2 immune response and improved intestinal barrier function.
- Melatonin's protective effects were microbiota-dependent, altering gut microbial composition by increasing beneficial bacteria (e.g., Bifidobacterium) and decreasing harmful ones.
- FMT from melatonin-treated mice ameliorated colitis in recipient mice.
Conclusions:
- Melatonin ameliorates Oxa-induced colitis through a microbiota-dependent mechanism.
- Melatonin modulates gut microbiota composition and suppresses type 2 immunity.
- Melatonin shows therapeutic potential for type 2 immunity-associated UC.
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