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Published on: August 30, 2014
Quercetin restores respiratory mucosal barrier dysfunction in Mycoplasma gallisepticum-infected chicks by enhancing
Shun Wang1, Liyang Guo1, Fuhua Gu1
1College of Veterinary Medicine, Northeast Agricultural University, 600 Changjiang Road, Xiangfang District, Harbin 150030, PR China; Heilongjiang Key Laboratory for Animal Disease Control and Pharmaceutical Development, 600 Changjiang Road, Xiangfang District, Harbin 150030, PR China.
Background:
Mycoplasma gallisepticum (MG) has long been a pathogenic microorganism threatening the global poultry industry. Previous studies have demonstrated that the mechanism by which quercetin (QUE) inhibits the colonization of MG in chicks differs from that of antibiotics. However, the molecular mechanism by which QUE facilitates the clearance of MG remains unclear.
Purpose:
The aim of this study was to investigate the molecular mechanism of MG clearance by QUE, with the expectation of providing new options for the treatment of MG.
Methods:
A model of MG infection in chicks and MG-induced M1 polarization in HD-11 cells were established. The mechanism of QUE clearance of MG was investigated by evaluating the relationship between tracheal mucosal barrier integrity, antibody levels, Th1/Th2 immune balance and macrophage metabolism and M1/M2 polarization balance. Furthermore, network pharmacology and molecular docking techniques were employed to explore the potential molecular pathways connecting QUE, M2 polarization, and fatty acid oxidation (FAO).
Results:
The findings indicate that QUE remodels tracheal mucosal barrier function by regulating tight junctions and secretory immunoglobulin A (sIgA) expression levels. This process entails the regulatory function of QUE on the Th1/Th2 immune imbalance that is induced by MG infection in the tracheal mucosa. Moreover, QUE intervention impeded the M1 polarization of HD-11 cells induced by MG infection, while simultaneously promoting M2 polarization through the induction of FAO. Conversely, inhibitors of the FAO pathway impede this effect. The results of computer network analysis suggest that QUE may induce FAO via the PI3K/AKT pathway to promote M2 polarization. Notably, inhibition of the PI3K/AKT pathway was found to effectively inhibit M2 polarization in HD-11 cells, while having a limited effect on FAO.
Conclusions:
QUE promotes M2 polarization of HD-11 cells to enhance Th2 immune response through FAO and PI3K/AKT pathways, thereby restoring tracheal mucosal barrier function and ultimately inhibiting MG colonization.
Insights
Quercetin (QUE) enhances the poultry immune response against Mycoplasma gallisepticum (MG) by promoting M2 macrophage polarization via fatty acid oxidation and PI3K/AKT pathways. This improves the tracheal mucosal barrier and inhibits MG colonization.
Area of Science:
- Veterinary Immunology
- Poultry Pathology
- Molecular Mechanisms of Disease
Background:
- Mycoplasma gallisepticum (MG) poses a significant threat to the global poultry industry.
- The precise molecular mechanisms by which quercetin (QUE) aids MG clearance are not fully understood, distinguishing its action from antibiotics.
Purpose of the Study:
- To elucidate the molecular pathways through which QUE facilitates the clearance of Mycoplasma gallisepticum.
- To explore QUE as a potential therapeutic agent for MG infections in poultry.
Main Methods:
- Establishing chick models of MG infection and HD-11 cell M1 polarization.
- Assessing tracheal mucosal barrier integrity, antibody levels, and Th1/Th2 immune balance.
- Investigating macrophage M1/M2 polarization, fatty acid oxidation (FAO), network pharmacology, and molecular docking.
Main Results:
- QUE restored tracheal mucosal barrier function by regulating tight junctions and secretory IgA (sIgA).
- QUE modulated the Th1/Th2 immune imbalance and promoted M2 macrophage polarization by inducing FAO, counteracting MG-induced M1 polarization.
- Network pharmacology suggested QUE induces FAO via the PI3K/AKT pathway, promoting M2 polarization.
Conclusions:
- Quercetin promotes M2 polarization of macrophages via FAO and PI3K/AKT pathways, enhancing the Th2 immune response.
- This action restores tracheal mucosal barrier function, leading to the inhibition of Mycoplasma gallisepticum colonization.
