Alanylglutamine Relieved Asthma Symptoms by Regulating Gut Microbiota and the Derived Metabolites in Mice

Oxid Med Cell Longev. 2020 Dec 29:2020:7101407. doi: 10.1155/2020/7101407. eCollection 2020.

Abstract

Objective: Allergic asthma is a chronic inflammatory disease, which seriously affects the life quality of patients, especially children. Alanylglutamine is a nutritional supplement with potential protective and anti-inflammatory effects, but its function in allergic asthma remains elusive. In this study, we focused on the investigations of the roles and functional mechanism of Alanylglutamine in asthma.

Methods: Ovalbumin (OVA) induction was utilized to establish a mouse asthma model. 16S rDNA sequencing was performed to compare the diversity of intestinal microorganisms under different treatments. Gas chromatography was utilized to screen the intestinal microbe-short-chain fatty acids in the stool. The lung tissue was extracted to determine signaling pathways, including AMPK, NF-κB, mTOR, STAT3, IKKβ, TGF-β, and IL-1β through Western blot or RT-qPCR.

Results: It was observed that Alanylglutamine reduced the cytokine in OVA-induced allergic asthma mice. H&E staining showed obvious pneumonia symptoms in the asthma group, while Alanylglutamine alleviated the inflammatory infiltration. Alanylglutamine reversed gut microbiota compositions in OVA-induced allergic asthma mice and enhanced the butyric acid level. The protective role of Alanylglutamine may be associated with the gut microbiota-butyric acid-GPR43 pathway in asthma mice. In contrast to the OVA group, Alanylglutamine activated the protein expression of P-AMPK/AMPK and inhibited the protein expression of P-mTOR/mTOR, P-P65/P65, P-STAT3/STAT3, P-IKKβ/IKKβ, TGF-β, and IL-1β, with similar effects from butyric acid.

Conclusion: The results indicated that Alanylglutamine might be beneficial for asthma, and its effect was achieved through the regulation on microbiota and the derived metabolites. The therapeutic effects might be associated with AMPK, NF-κB, mTOR, and STAT3 signaling pathways. These findings will help identify effective therapeutic direction to alleviate allergic inflammation of the lungs and airways.

MeSH terms

  • Amino Acids / analysis
  • Animals
  • Anti-Bacterial Agents / pharmacology
  • Asthma / complications
  • Asthma / drug therapy*
  • Asthma / microbiology*
  • Biodiversity
  • Butyric Acid / pharmacology
  • Cytokines / metabolism
  • Dipeptides / pharmacology
  • Dipeptides / therapeutic use*
  • Feces / microbiology
  • Gastrointestinal Microbiome* / drug effects
  • Hypersensitivity / complications
  • Hypersensitivity / microbiology
  • Inflammation / pathology
  • Male
  • Metabolome* / drug effects
  • Mice, Inbred BALB C
  • NF-kappa B / metabolism
  • Ovalbumin
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction

Substances

  • Amino Acids
  • Anti-Bacterial Agents
  • Cytokines
  • Dipeptides
  • NF-kappa B
  • STAT3 Transcription Factor
  • Butyric Acid
  • Ovalbumin
  • alanylglutamine