Abstract
Exposure of the respiratory tract of an atopic individual to allergens such as D. pteronyssinus (DP) house dust mite is associated with the development of allergic asthma. In the study, we explored the role of Toll-like receptors (TLRs) in allergen-induced inflammatory responses of human bronchial epithelial cells. Our results showed that DP induced production of G-CSF, GM-CSF, CXCL1, IL-6, CXCL8, and CCL2 in BEAS-2B (immortalized human bronchial epithelial cells) in a dose-dependent manner. An inhibitory peptide against MyD88 significantly inhibited the allergen-induced cytokine response, while monoclonal antibodies (mAbs) against TLR2 showed some (but not significant) inhibitory effects. Analysis of mRNA transcripts by qPCR revealed an increased expression of MyD88 at 1 hr post-stimulation with DP. DP stimulation also induced increased expression of TLR1, TLR2, TLR3, TLR5, TLR8, and TLR9, as well as IFNβ. HKLM, a TLR2 agonist, along with DP showed a synergistic effect on cytokine response of BEAS-2B and the response was inhibited by anti-TLR2 mAb. HEK293 cells expressing TLR1/2, TLR2/6 or TLR4/CD14/MD2 showed increased cytokine response to allergens, while anti-TLR2 inhibited the response in HEK293 cells expressing TLR1/2 or TLR2/6. These data demonstrate a link between DP allergen-induced inflammatory response and TLR2-mediated signaling in airway epithelial cells and contribute to our understanding of the role of innate immunity in allergic diseases.