Mahuang Fuzi Xixin decoction attenuates allergic rhinitis by suppressing MHC-II-mediated antigen presentation in ovalbumin induced murine model
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Xiaohan Wei1, Mengze Ding2, Xiaomei Tan2
1Department of Pharmacy, Personalized Drug Research and Therapy Key Laboratory of Sichuan Province, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China; School of Traditional Chinese Medicine, Southern Medical University, Guangzhou Guangdong 510515, China.
Background:
Allergic rhinitis (AR) is a chronic condition that impairs daily life and imposes economic burdens. Mahuang Fuzi Xixin Decoction (MFXD) is a commonly employed herbal formula in China for treating AR, owing to its established clinical efficacy. However, investigations into its underlying mechanisms remain limited.
Purpose:
To evaluate the therapeutic effects of MFXD in a mouse model of AR and to investigate its influence on antigen presentation, thereby elucidating potential mechanisms of action.
Materials And Methods:
An ovalbumin (OVA)-induced murine AR model was established to assess the efficacy of MFXD. Subsequently, data-independent acquisition (DIA) proteomics characterized differentially expressed proteins (DEPs) in the nasal mucosa following MFXD treatment, followed by pathway enrichment analysis. Guided by the proteomic findings, we examined the regulatory effects of MFXD on antigen presentation molecules in AR mice. Finally, human nasal epithelial cells (HNEpCs), dendritic cells (DC2.4), and Naïve CD4+ T cells isolated from OT-II mice were used to confirm the inhibitory effect of MFXD on the antigen presentation pathway. Additionally, chemical characterization of MFXD was performed.
Results:
MFXD alleviated AR symptoms, mitigated histopathological alterations, and regulated plasma histamine and IgE levels, as well as IL-4, IL-13, and IFN-γ levels in the nasal lavage fluid (NLF) in AR mice. MFXD significantly reduced the number of nasal DEPs between AR and control groups, with the antigen processing and presentation pathway being the most prominently enriched. MFXD modulated splenic histopathology and spleen index, and decreased major histocompatibility complex class II (MHC-II) expression in both the nasal mucosa and spleen of AR mice. In vitro, MFXD diminished the antigen phagocytic capacity of lipopolysaccharide (LPS)-stimulated DC2.4 cells and lowered MHC-II and CD86 expression on both HNEpCs and DC2.4 cells; It also suppressed DC2.4-induced proliferation and differentiation of naive OT-II CD4+ T cells. MFXD also downregulated CD74, cathepsin S (CTSS), and MHC-II; this effect was partially reversed by the CD74 agonist MIF and by CD74 overexpression.
Conclusions:
This study explores one potential therapeutic mechanism of MFXD in AR. The findings suggests that MFXD may exert its therapeutic effect against AR by suppressing CD74/CTSS/MHC-II axis, thereby inhibiting antigen presentation. This work provides mechanistic insights that could inform the clinical use of MFXD and highlights potential targets for future AR drug development.
Compound:
Ephedrine, Pseudoephedrine, Methylephedrine, Benzoylmesaconine, Benzoylhypacoitine, Benzoylaconine, Asarone.
