Iloprost inhibits acute allergic nasal inflammation by GATA3 -ILC2 pathway in mice

Abstract

BackgroundAcute allergic nasal inflammation is very common in the clinical allergic diseases, Prostaglandin I2 (PGI2) has been found to effective in combating inflammation. Iloprost, as an analog of PGI2, whose role and mechanisms in the acute allergic nasal inflammation remains unclear. It’s necessary to elucidate the efficacy and potential mechanism of Iloprost in acute allergic nasal inflammation. Methods36 female mice were randomly divided into DMSO group, IL 33 group, Iloprost group and IL 33+Iloprost intervention group. Mice were stimulated with IL 33 to construct an acute allergic nasal inflammation model. Hematoxylin and eosin (HE) and periodic acid Schiff reagent (PAS) staining, flow cytometry, Real time PCR and Enzyme linked immunosorbent assay (ELISA) was used to identify the role of Iloprost in acute allergic nasal inflammation. The comparison between multiplied groups was analyzed by ANOVA, and the Bonferroni method was used for further comparison of two groups. ResultsCompared with IL 33 group, the inflammatory cell infiltration around the trachea and blood vessels of the lung tissue in the IL 33+ Iloprost group were reduced; goblet cell hyperplasia was observed in airway mucosa of IL 33 group, and the mucus secretion increased; the percentage of EOS and ILC2s in the BALF and lung single cell suspensions in IL 33+ Iloprost group were statistically lower than that of IL 33 group (p < 0.05); The mRNA expression levels of IL 5, IL 13, ST2 and GATA3 in the lung tissue of IL 33 group were higher than those in DMSO group (p < 0.05). After intervention with Iloprost, the mRNA expression levels of IL 5, IL 13, GATA3 and ST2 were lower than those in IL 33 group (p < 0.05) ConclusionIloprost may potentially inhibit the proliferation and activation of innate lymphoid cells 2 in mice with acute allergic inflammation, which maybe an effective option for the treatment of acute allergic inflammation related diseases.