BackgroundThe prevalence of allergic diseases such as asthma has significantly increased worldwide, making it a public health concern. There is an urgent need for new anti-inflammatory agents with selective pharmacology and lower toxicity. Plant extracts have been used for centuries in traditional medicine to alleviate inflammatory diseases. In this work, we evaluated the anti-allergic activity of Cymbopogon citratus (Cy), a medicinal herb used by folk medicine to treat asthma.MethodsWe used a murine model of respiratory allergy to the mite Blomia tropicalis (Bt) and evaluated certain parameters known to be altered in this model. A/J mice were sensitized (100 μg/animal s.c.) and challenged (10 μg/animal i.n.) with Bt mite extract and treated with 60, 120 or 180 mg/kg of Cy standardized hexane extract. The parameters evaluated included: cellular infiltrate in bronchoalveolar lavage (BAL); eosinophil peroxidase activity (EPO); histopathological examination of the lung; serum levels of specific IgE, IgG1 and IgG2a; Th2 cytokine concentrations in BAL and expression of NF-κB.ResultsOur results showed that oral administration of a Cy hexane extract (especially 180 mg/Kg) reduced the numbers of leukocytes/eosinophils in BAL; the eosinophil peroxidase activity in BAL; the infiltration of leukocytes in lung tissue; the production of mucus in the respiratory tract; the level of IL-4 in BAL and the nuclear expression of NF-κB.ConclusionsThe results presented demonstrate the potential of the Cy hexane extract to modulate allergic asthma; this extract may be an alternative future approach to treat this pathology.
RATIONALE: Aryl hydrocarbon receptor (AhR), a receptor for common environmental contaminants, is an important regulator of immune responses. Our previous studies have suggested a role of AhR in protecting against cockroach allergen-induced lung inflammation by using AhR-/mice. Autophagy plays a major role in controlling immune responses and inflammation. We sought to determine whether the activated AhR signaling specifically in airway epithelium by cockroach allergen modulates cockroach allergen-induced lung inflammation through autophagy METHODS: The role of AhR expressed in epithelium in cockroach allergen (CRE) induced allergic inflammation was investigated in a mouse model of asthma with AhR epithelial conditional knock out mice (ftpc-Cre;AhR flox/flox). Cockroach allergen induced the activation of AhR and autophagy signaling in epithelium was determined. The role of autophagy in CRE-induced asthma was also investigated. RESULTS: CRE-challenged Sftpc-Cre; AhR flox/flox mice displayed decreased lung infiltrates, mucus production, and airway hyper-responsiveness. These mice also showed reduced levels of IL-4, IL-5, IL-13, IL-17, but increased IL-10 and IL-22 in the BAL fluids. Decreased IC3B II in airways was also observed. Moreover, CRE can activate AhR (CYP1A1 and CYP1B1) and autophagy (Beclin-1, Atg5, and p62) signaling in epithelial cells in vitro, and AhR agonist TCDD can potentiate CRE-induced autophagy. Furthermore, CRE-induced lung inflammation was significantly suppressed when autophagy inhibitor was used in the mouse model with decreased lung infiltrates and Th2/T17 cytokines in BAL fluids. CONCLUSIONS: Contrast to the protective role previously observed in AhR-/mice, AhR in airway epithelial may exacerbate CRE-induced inflammation, which may through activating autophagy signaling.
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