Abstract
Picroside II isolated from Pseudolysimachion rotundum var. subintegrum has been used as traditional medicine to treat inflammatory diseases. In this study, we assessed whether picroside II has inhibitory effects on airway inflammation in a mouse model of house dust mite (HDM)-induced asthma. In the HDM-induced asthmatic model, picroside II significantly reduced inflammatory cell counts in the bronchoalveolar lavage fluid (BALF), the levels of total immunoglobulin (Ig) E and HDM-specific IgE and IgG1 in serum, airway inflammation, and mucus hypersecretion in the lung tissues. ELISA analysis showed that picroside II down-regulated the levels of Th2-related cytokines (including IL-4, IL-5, and IL-13) and asthma-related mediators, but it up-regulated Th1-related cytokine, IFNγ in BALF. Picroside II also inhibited the expression of Th2 type cytokine genes and the transcription factor GATA3 in the lung tissues of HDM-induced mice. Finally, we demonstrated that picroside II significantly decreased the expression of GATA3 and Th2 cytokines in developing Th2 cells, consistent with in vivo results. Taken together, these results indicate that picroside II has protective effects on allergic asthma by reducing GATA3 expression and Th2 cytokine bias.
Highlights
Allergic asthma is a chronic inflammatory disease characterized by infiltration of the airway wall with eosinophils and CD4+ T helper type 2 (Th2) cells, reversible airway obstruction, airway hyper-responsiveness (AHR), mucus hypersecretion and airway remodeling [1, 2]
We first compared the effects of YPL-001 and picroside II on airway inflammation by counting inflammatory cells in bronchoalveolar lavage fluid (BALF)
We have compared the extent of inhibition by picroside II and YPL-001 on allergic airway inflammation by analyzing the inflammatory cells in BALF of the house dust mite (HDM)-treated mice
Summary
Allergic asthma is a chronic inflammatory disease characterized by infiltration of the airway wall with eosinophils and CD4+ T helper type 2 (Th2) cells, reversible airway obstruction, airway hyper-responsiveness (AHR), mucus hypersecretion and airway remodeling [1, 2]. House dust mite (HDM) is the most prevalent cause of allergic sensitization [4, 6], and a risk factor for persistent asthma in human subjects [7, 8]. The appropriate differentiation of these CD4+ T-cell subsets requires activation of transcription factors, including signal transducers and activators of transcription (STATs) [11]. GATA3 induces Th2 cell development by promoting Th2 cytokine expression, but simultaneously inhibits Th1 differentiation by inhibiting T-bet and plays a critical role in asthma [14, 16, 17]. Excessive cytokines IL-4, IL-5, and IL-13 produced by Th2 cells are significant risk factors in asthma pathogenesis [19]. Suppression of overproduced Th2 cytokines is important for the treatment of the disease
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
