Inhibitory Effect of Propofol on Type II Inflammation in Mice with Allergic Rhinitis

Propofol, a quick‑acting systemic anesthetic agent widely used in general anesthesia, can alleviate airway T-helper 2 (TH2) inflammation. Group 2 innate lymphoid cells (ILC2s) are a newly discovered group of lymphoid cells and play key roles in allergic rhinitis (AR). We aimed to investigate the regulation of ILC2s treated with propofol and its possible mechanisms in a mouse model. An ovalbumin (OVA)-sensitized and challenged mouse model was established. Nasal lavage fluid (NLF) and tissue samples were collected for the detection of inflammatory cells, type II cytokines, and ILC2s using Giemsa staining, enzyme-linked immunosorbent assay, and flow cytometry. CD4+ T cells and ILC2s were cocultured and detected by flow cytometry to confirm the proportion of TH2 cells. Compared with OVA-sensitized and challenged mice, propofol-treated model mice presented decreased type II cytokine levels and total numbers of cells, eosinophils, neutrophils, and macrophages in NLF. Mice treated with propofol presented decreased nasal ILC2 frequency. Moreover, the nasal expression of GATA binding protein 3 (GATA3) and retinoid-related orphan receptor α (RORα), as well as the levels of IL-5 and IL-13, were significantly inhibited after propofol treatment. Compared with those cultured alone, cocultures of ILC2s and CD4+ T cells resulted in significantly more TH2 cells. When propofol was added, the percentage of TH2 cells significantly decreased. This effect was alleviated when anti-major histocompatibility complex class II (anti-MHC II) protein was added. Our study provides preliminary evidence that propofol can play an inhibitive role in AR by regulating innate and adaptive immunity.