Rebalancing the inflammatory niche in allergic rhinitis ".
Abstract
Allergic rhinitis (AR) may be driven in part by cross-talk between resident microbiota, microbe-derived small molecules, and tissue-resident group 2 innate lymphoid cells (ILC2s). In this review we focus on defined signaling axes by which Traditional Chinese Medicine (TCM) can influence that network: (1) microbially produced short-chain fatty acids (SCFAs), particularly butyrate, suppress ILC2 proliferation and type-2 cytokine output primarily via HDAC inhibition that downregulates the lineage transcription factor GATA3; receptor-dependent effects via the SCFA sensors FFAR3 (GPR41), FFAR2 (GPR43), and GPR109A (HCAR2) also occur in some cell types and tissues, and can engage β-arrestin/ERK or AMPK-linked pathways depending on cell context. In purified ILC2s, ex-vivo reductions in GATA3 and IL-13/IL-5 are observed at low micromolar to several hundred micromolar butyrate (human ILC2 ≈ 10 μM; murine ex-vivo ILC2 ≈ 200 μM), while viability is generally preserved below ∼1 mM, indicating a physiologically plausible dose window for metabolite-driven modulation; (2) microbially modified secondary bile acids alter mucosal immune tone and epithelial function via FXR and TGR5 signaling; and (3) microbial tryptophan metabolites (indoles) act as aryl hydrocarbon receptor (AhR) ligands that preserve epithelial integrity and shape ILC3/ILC2 balance. We review preclinical and emerging clinical data suggesting that selected TCM formulas and phytochemicals (e.g., Gegen Qinlian Decoction,…
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