Short-term administration of Qipian?, a mixed bacterial lysate, inhibits airway inflammation in ovalbumin-induced mouse asthma by modulating cellular, humoral and neurogenic immune responses

Aims Qipian? is a commercialized agent composed of extracts of three genera of commensal bacteria, and its mechanism of action on asthma is unclear. This study aimed to examine the impact of Qipian? on airway inflammation and investigate the underlying mechanisms. Materials and methods Qipian? or dexamethasone (DEX) was administered before OVA challenge in an ovalbumin-induced asthma mouse model, and then asthmatic symptoms were observed and scored. Samples of lung tissues, blood, and bronchoalveolar lavage fluid (BALF) were collected, and eosinophils (Eos), immunoglobins (Igs), and type 1?T helper (Th1)/Th2 cell cytokines were measured. Mucus production in the lung was assessed by periodic acid-Schiff (PAS) staining. The effects of Qipian? on dendritic and T regulatory (Treg) cells were investigated using flow cytometry. Key findings The short-term administration of Qipian? significantly inhibited the cardinal features of allergic asthma , including an elevated asthmatic behaviour score, airway inflammation and immune response. Histological analysis of the lungs showed that Qipian? attenuated airway inflammatory cell infiltration and mucus hyperproduction. Qipian? restored Th1/Th2 imbalance by decreasing interleukin (IL)-4, IL-5, and IL-13 while increasing interferon (IFN)-γ and IL-10. Further investigation revealed that Qipian? treatment induced the upregulation of CD4 + CD25 + Foxp3 + Treg cells and CD103 + DCs and downregulation of tachykinins neurokinin A (NKA) and NKB in the lung. Significance Our findings suggested that short-term treatment with Qipian? could alleviate inflammation in allergic asthma through restoring the Th1/Th2 balance by recruiting Treg cells to airways and inducing the proliferation of CD103 + DCs, which actually provides a new treatment option for asthma.

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