DEC2 deficiency promotes high incidence of cough after infection and the therapeutic mechanism of ephedrine hydrochloride

The absence of DEC2 exacerbated LPS-induced pulmonary inflammatory response, especially increased expression of IL-1, IL-6, γ-interferon receptor (IFNGR), IL-1R, IL-6R in lung CD45- cells (P<0.01), and activation of P65 was promoted (P<0.01).After EH treatment, the cough frequency in DEC2-KO PIC mice was significantly reduced (P<0.001), the expression of IL-1, IL-6, IFN-γ in lung and IL-1R, IL-6R, IFNGR in pulmonary CD45-cells were down-regulated (P<0.01).

The expression and activation of NF-kB induced by DEC2 deletion were significantly inhibited (P<0.01).Conclusion The deficency of DEC2 can activate NFKB signal and promote the high expression of inflammatory cytokine and receptors in pulmonary CD45-cells, which is a risk factor in the high incidence of PIC. EH can inhibit the excessive-activation of NFkB signal and the inflammatory characteristics of lung local stromal cells caused by DEC2 absence, and that is the main part of pharmacological mechanism for effective treatment of EH targeting PIC.