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Published on: June 23, 2013
L-arabinose Attenuates LPS-Induced Intestinal Inflammation and Injury through Reduced M1 Macrophage Polarization
Luyuan Kang1, Jiaman Pang1, Xiangyu Zhang1
1State Key Laboratory of Animal Nutrition and Feeding, College of Animal Science and Technology, China Agricultural University, Beijing, China.
Background:
L-arabinose has anti-inflammatory and metabolism-promoting properties, and macrophages participate in the alleviation of inflammation; however, the mechanism by which they contribute to the anti-inflammatory effects of L-arabinose is unknown.
Objectives:
To investigate the involvement of macrophages in the mitigation of L-arabinose in an intestinal inflammation model induced by lipopolysaccharide (LPS).
Methods:
Five-week-old male C57BL/6 mice were divided into 3 groups: a control and an LPS group that both received normal water supplementation, and an L-arabinose (ARA+LPS) group that received 5% L-arabinose supplementation. Mice in the LPS and ARA+LPS groups were intraperitoneally injected with LPS (10 mg/kg body weight), whereas the control group was intraperitoneally injected with the same volume of saline. Intestinal morphology, cytokines, tight junction proteins, macrophage phenotypes, and microbial communities were profiled at 6 h postinjection.
Results:
L-arabinose alleviated LPS-induced damage to intestinal morphology. L-arabinose down-regulated serum tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6, and messenger RNA (mRNA) levels of TNF-α, IL-1β, interferon-γ (IFN-γ), and toll-like receptor-4 in jejunum and colon compared with those of the LPS group (P < 0.05). The mRNA and protein levels of occludin and claudin-1 were significantly increased by L-arabinose (P < 0.05). Interferon regulatory factor-5 (IRF-5) and signal transducer and activator of transcription-1 (STAT-1), key genes characterized by M1 macrophages, were elevated in the jejunum and colon of LPS mice (P < 0.05) but decreased in the ARA+LPS mice (P < 0.05). In vitro, L-arabinose decreased the proportion of M1 macrophages and inhibited mRNA levels of TNF-α, IL-1β, IL-6, IFN-γ, as well as IRF-5 and STAT-1 (P < 0.01). Moreover, L-arabinose restored the abundance of norank_f__Muribaculaceae, Faecalibaculum, Dubosiella, Prevotellaceae_UCG-001, and Paraasutterella compared with those of LPS (P < 0.05) and increased the concentration of short-chain fatty acids (P < 0.05).
Conclusion:
The anti-inflammatory effects of L-arabinose are achieved by reducing M1 macrophage polarization, suggesting that L-arabinose could be a candidate functional food or nutritional strategy for intestinal inflammation and injury.
Insights
L-arabinose reduces intestinal inflammation by decreasing M1 macrophage polarization. This study suggests L-arabinose as a potential nutritional strategy for managing gut inflammation and injury.
Area of Science:
- Immunology
- Gastroenterology
- Nutritional Science
Background:
- L-arabinose exhibits anti-inflammatory and metabolism-promoting properties.
- Macrophages play a role in inflammation resolution, but their specific involvement in L-arabinose's anti-inflammatory effects remains unclear.
Purpose of the Study:
- To investigate the role of macrophages in mediating the anti-inflammatory effects of L-arabinose in a lipopolysaccharide (LPS)-induced intestinal inflammation model.
Main Methods:
- C57BL/6 mice were administered L-arabinose or saline before LPS injection.
- Intestinal morphology, cytokine profiles, tight junction proteins, macrophage phenotypes (M1 polarization markers IRF-5 and STAT-1), and gut microbiota were analyzed.
Main Results:
- L-arabinose mitigated LPS-induced intestinal damage and reduced pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IFN-γ).
- L-arabinose increased tight junction proteins (occludin, claudin-1) and decreased M1 macrophage markers.
- L-arabinose modulated gut microbiota composition and increased short-chain fatty acid levels.
Conclusions:
- L-arabinose exerts anti-inflammatory effects by inhibiting M1 macrophage polarization.
- L-arabinose shows potential as a functional food or nutritional intervention for intestinal inflammation and injury.
