The Mediation Effects Of Th17in Mice Asthma Model Induced By DEHP

DEHP as the most widely used plasticizer, was easily released into the environment and was a usual environmental pollutant. DEHP exposure could cause a variety of toxic and harms to human health, recent studies showed that there was a certain relationship between DEHP and allergic diseases. The concentration of DEHP in indoor dust was related to children asthma and syndrome like asthma. Studies on asthma induced by DEHP always began with the Th1/Th2traditional approach. While another novel CD4+T lymphocyte effector Th17was discovered, the effects of Th17in inflammation attracted more and more attentions. To explore the role of Th17cells in the pathogenesis of mouse asthma model induced by DEHP, this study tested the changes of IL-17in the relevant tissues, based on the mouse asthma model.BalB/c mice were randomly divided into four groups, with each group containing6mice:untreated control group, DEHP exposure group, OVA sensitized group and DEHP and OVA combined exposure group. The mouse asthma model was developed by OVA sensitization and challenge. The DEHP exposure group was given10mg/kg/day DEHP daily by gavaging for54consecutive days. The OVA exposure group and DEHP+OVA exposure group were given aerosol challenges with1%OVA (30min/day) for a week to induce the asthma syndrome. On the60th day, lung function testing, bronchoalveolar lavage fluid (BALF) collection, serum collection, and lung tissue homogenate preparation were undertaken. The biomarkers mainly included indicators related to mouse asthma model and the IL-17in lung tissue. Compared with OVA exposure group, Ri and Re of DEHP+OVA exposure group were significantly increased, the ratio of eosinophils to total cells and the T-IgE level were all enhanced significantly, which showed that DEHP could improve the development of asthma symptoms; Compared with saline group, the IL-17levels in lung and BALF were both increased significantly (p<0.05) in DEHP exposure group. It suggested that the asthma induced by DEHP might be mediated by Th17.Comprehensive analysis of the above experimental results, it was easy to found that DEHP had impacts on the occurrence of asthma. We could guess the following conclusions:Firstly, DEHP was involved in the mouse asthma, as a role of similar immune’adjuvant’, which could be supported by the data of DEHP+OVA combined exposure group when compared with OVA group, T-IgE in serum, AHR and ratio of EOS in BALF were all increased significantly. What’s more, changes of IL-4and IFN-y levels showed that the Th1and Th2populations played a role in the procession and the balance of Th1/Th2was broken and tended to Th2populations, this was consistent to the previous researches. At last, when compared with saline group, the IL-17levels of DEHP group and DEHP+OVA group in lung and BALF had a significant rise, which also proved Th17populations, just like the Th2populations, promoted inflammation by increasing differentiation. So the traditional issue, the balance of Thl/Th2, was not prefect, to be more precise, it was that DEHP might be promote inflammation process involves of Thl, Th2and Th17three types of cell populations.