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J Agric Food Chem ; 72(17): 9782-9794, 2024 May 01.
Article in English | MEDLINE | ID: mdl-38597360

ABSTRACT

Uncontrolled inflammation contributes significantly to the mortality in acute respiratory infections. Our previous research has demonstrated that maize bran feruloylated oligosaccharides (FOs) possess notable anti-inflammatory properties linked to the NF-kB pathway regulation. In this study, we clarified that the oral administration of FOs moderately inhibited H1N1 virus infection and reduced lung inflammation in influenza-infected mice by decreasing a wide spectrum of cytokines (IFN-α, IFN-ß, IL-6, IL-10, and IL-23) in the lungs. The mechanism involves FOs suppressing the transduction of the RIG-I/MAVS/TRAF3 signaling pathway, subsequently lowering the expression of NF-κB. In silico analysis suggests that FOs have a greater binding affinity for the RIG-I/MAVS signaling complex. This indicates that FOs have potential as promising targets for immune modulation. Moreover, in MAVS knockout mice, we confirmed that the anti-inflammatory function of FOs against influenza depends on MAVS. Comprehensive analysis using 16S rRNA gene sequencing and metabolite profiling techniques showed that FOs have the potential to restore immunity by modulating the gut microbiota. In conclusion, our study demonstrates that FOs are effective anti-inflammatory phytochemicals in inhibiting lung inflammation caused by influenza. This suggests that FOs could serve as a potential nutritional strategy for preventing the H1N1 virus infection and associated lung inflammation.


Subject(s)
DEAD Box Protein 58 , Influenza A Virus, H1N1 Subtype , Influenza, Human , Mice, Knockout , Oligosaccharides , Orthomyxoviridae Infections , Signal Transduction , TNF Receptor-Associated Factor 3 , Animals , Mice , Oligosaccharides/administration & dosage , Oligosaccharides/chemistry , Oligosaccharides/pharmacology , Orthomyxoviridae Infections/immunology , Orthomyxoviridae Infections/prevention & control , Orthomyxoviridae Infections/metabolism , Influenza A Virus, H1N1 Subtype/immunology , Humans , Signal Transduction/drug effects , Signal Transduction/immunology , Influenza, Human/immunology , Influenza, Human/prevention & control , Influenza, Human/metabolism , TNF Receptor-Associated Factor 3/genetics , TNF Receptor-Associated Factor 3/metabolism , TNF Receptor-Associated Factor 3/immunology , DEAD Box Protein 58/genetics , DEAD Box Protein 58/metabolism , DEAD Box Protein 58/immunology , Pneumonia/immunology , Pneumonia/prevention & control , Pneumonia/metabolism , Pneumonia/virology , Mice, Inbred C57BL , Lung/immunology , Lung/metabolism , Lung/drug effects , Lung/virology , Cytokines/metabolism , Cytokines/immunology , Cytokines/genetics , Female , NF-kappa B/immunology , NF-kappa B/genetics , NF-kappa B/metabolism , Anti-Inflammatory Agents/administration & dosage , Anti-Inflammatory Agents/pharmacology
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