Abstract
Illicium verum is used in traditional medicine to treat inflammation. The study investigates the effects of IVE and its component, trans-anethole (AET), on airway inflammation in ovalbumin- (OVA-) induced asthmatic mice. Asthma was induced in BALB/c mice by systemic sensitization to OVA, followed by intratracheal, intraperitoneal, and aerosol allergen challenges. IVE and AET were orally administered for four weeks. We investigated the effects of treatment on airway hyperresponsiveness, IgE production, pulmonary eosinophilic infiltration, immune cell phenotypes, Th2 cytokine production in bronchoalveolar lavage, Th1/Th2 cytokine production in splenocytes, forkhead box protein 3 (Foxp3) expression, and lung histology. IVE and AET ameliorated OVA-driven airway hyperresponsiveness (p < 0.01), pulmonary eosinophilic infiltration (p < 0.05), mucus hypersecretion (p < 0.01), and IL-4, IL-5, IL-13, and CCR3 production (p < 0.05), as well as IgE levels (p < 0.01). IVE and AET increased Foxp3 expression in lungs (p < 0.05). IVE and AET reduced IL-4 and increased IFN-γ production in the supernatant of splenocyte cultures (p < 0.05). Histological studies showed that IVE and AET inhibited eosinophilia and lymphocyte infiltration in lungs (p < 0.01). These results indicate that IVE and AET exert antiasthmatic effects through upregulation of Foxp3+ regulatory T cells and inhibition of Th2 cytokines, suggesting that IVE may be a potential therapeutic agent for allergic lung inflammation.
Highlights
Allergic asthma is caused by a T helper cell type 2- (Th2-) mediated immune response to common environmental allergens and is defined by chronic inflammatory lung disease
We previously found that topical application of I. verum extract (IVE) improved dermatitis in house dust mite-induced NC/Nga mice by modulating the level of IgE and Th2 cytokines and chemokines [14]
We found that the Penh dose-response curve was shifted to the left in Ovalbumin Penh (OVA)-induced asthmatic mice, compared to normal mice (Figure 1(b))
Summary
Allergic asthma is caused by a T helper cell type 2- (Th2-) mediated immune response to common environmental allergens and is defined by chronic inflammatory lung disease. Multiple cell types, including mast cells, eosinophils, basophils, neutrophils, and Th2 lymphocytes, contribute to the pathogenesis of asthma by producing cytokines like interleukin- (IL-) 4, IL-5, and IL-13 [4]. Increased eosinophil and T lymphocyte numbers in bronchoalveolar lavage fluid (BALF) and bronchial mucosa are characteristic features of the inflammatory response in asthmatic patients and correlate with the severity of the disease [5]. IL-4 and IL-13 play critical roles in immunoglobulin (Ig) E isotype switching in B cells, eosinophil infiltration into lung tissues, and mucus hypersecretion [6]. Interferon- (IFN-) γ, which is produced by Th1 cells, regulates eosinophil recruitment in the airway by inhibiting the Th2 response [8]
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