NOD1 mediated D. pteronyssinus-induced allergic airway inflammation through RIP2/NF-κB.

Background: Dermatophagoides pteronyssinus (D. pteronyssinus) is the main cause of allergic airway inflammation. As the earliest intracytoplasmic pathogen recognition receptors (PRR), NOD1 has been identified as key inflammatory mediator in NOD-like receptor (NLR) family.

Objective: Our primary aim is to elucidate whether NOD1 and its downstream regulatory proteins mediate D. pteronyssinus-induced allergic airway inflammation.

Methods: Mouse and cell models of D. pteronyssinus-induced allergic airway inflammation were established. NOD1 was inhibited in bronchial epithelium cells (BEAS-2B cells) and mice by cell transfection or application of inhibitor. The change of downstream regulatory proteins was detected by quantitative real-time PCR (qRT-PCR) and Western blot. The relative expression of inflammatory cytokines was evaluated by ELISA.

Results: The expression level of NOD1 and its downstream regulatory proteins increased in BEAS-2B cells and mice after treating with D. pteronyssinus extract, followed by the aggravation of inflammatory response. Moreover, inhibition of NOD1 decreased the inflammatory response, which also downregulated the expression of downstream regulatory proteins and inflammatory cytokines.

Conclusions: NOD1 involves in the development of D. pteronyssinus-induced allergic airway inflammation. Inhibition of NOD1 reduces D. pteronyssinus-induced airway inflammation.