title: [Estrogen shortens the latent period of inducing asthma and promotes airway inflammation].
abstract: Objective To investigate the effect of estrogen on the latent period of inducing asthma and airway inflammation in mice with asthma. Methods Forty male BALB/c mice were randomly divided into normal control group, OVA-induced asthma group, 400 μg/kg estradiol treatment group, 400 μg/kg estradiol combined with 7 mg/kg tamoxifen group, with 10 mice in each group. The OVA-induced asthma group, estradiol treatment group, and estradiol combined with tamoxifen group were sensitized and challenged by OVA; the normal control group was treated with normal saline instead. The estradiol treatment group and estradiol combined with tamoxifen group were given intraperitoneal injection of 400 μg/kg estradiol 4 hours before each challenge, and the latter was given additionally intraperitoneal injection of 7 mg/kg tamoxifen at 30 minutes before the injection of estradiol; the normal control group and OVA-induced asthma group were injected with normal saline as controls. The latent period of inducing asthma of all the mice was determined 24 hours after the final OVA challenge. Bronchoalveolar lavage fluid (BALF) was collected for counting total leukocyte cells and the percentages of eosinophils and lymphocytes. The concentrations of interleukin 4 (IL-4) and IL-13 in BALF were detected by ELISA. The pathologic change of lung tissues was examined by HE staining. Results Compared with the normal control group, the latent period of inducing asthma were shortened in the OVA-induced asthma group, estradiol treatment group, and estradiol combined with tamoxifen group; compared with the OVA-induced asthma group and estradiol combined with tamoxifen group, the latent period of inducing asthma of the estradiol treatment group were shortened; there was no significant difference in the latent period between the OVA-induced asthma group and the estradiol combined with tamoxifen group. Compared with the normal control group, the levels of IL-4 and IL-13 increased in the OVA-induced asthma group, estradiol treatment group, and estradiol combined with tamoxifen group; compared with the OVA-induced asthma group and estradiol combined with tamoxifen group, the levels of IL-4 and IL-13 increased in the estradiol treatment group; there was also no significant difference between the OVA-induced asthma group and the estradiol combined with tamoxifen group. Compared with the normal control group, the total leukocytes and the percentages of eosinophils and lymphocytes in BALF were raised in the OVA-induced asthma group, estradiol treatment group, and estradiol combined with tamoxifen group; compared with OVA-induced asthma group and estradiol combined with tamoxifen group, the total leukocytes and the percentage of eosinophils and lymphocytes of BALF were elevated in the estradiol treatment group; there was no significant difference between the OVA-induced asthma group and the estradiol combined with tamoxifen group. There was no infiltration of inflammatory cells in bronchial walls or airway mucosal edema in the normal control group. There were infiltration of inflammatory cells in bronchial walls and airway mucosal edema in the OVA-induced asthma group and estradiol combined with tamoxifen group, in addition, the estradiol treatment group was more serious than the two groups in these pathologic changes. Conclusion Estrogen can shorten the latent period of inducing asthma, promote the airway inflammatory cell infiltration and upgrade the expressions of IL-4 and IL-13.
authors.affiliation: Department of Respiratory Medicine, Affiliated Hospital, Xuzhou Medical University, Xuzhou 221006, China.
authors.forename: Shuai
authors.initials: S
authors.lastname: Feng
authors.affiliation: Department of Respiratory Medicine, Affiliated Hospital, Xuzhou Medical University, Xuzhou 221006, China. *Corresponding author, E-mail: jiechenz356@sohu.com.
authors.forename: Shuyang
authors.initials: S
authors.lastname: Zhu
authors.affiliation: Department of Respiratory Medicine, Affiliated Hospital, Xuzhou Medical University, Xuzhou 221006, China.
authors.forename: Fangfang
authors.initials: F
authors.lastname: Han
authors.affiliation: Department of Respiratory Medicine, Affiliated Hospital, Xuzhou Medical University, Xuzhou 221006, China.
authors.forename: Jiechen
authors.initials: J
authors.lastname: Zhu
authors.affiliation: Department of Respiratory Medicine, Affiliated Hospital, Xuzhou Medical University, Xuzhou 221006, China.
authors.forename: Maowei
authors.initials: M
authors.lastname: Zhang
authors.affiliation: Department of Respiratory Medicine, Affiliated Hospital, Xuzhou Medical University, Xuzhou 221006, China.
authors.forename: Wengjing
authors.initials: W
authors.lastname: Liu
mesh_terms: D000818:Animals; D001249:Asthma / Q000209:etiology / Q000235:genetics / Q000276:immunology*; D001980:Bronchi / Q000276:immunology; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology; D004967:Estrogens / Q000276:immunology*; D005260:Female; D006801:Humans; D018793:Interleukin-13 / Q000235:genetics / Q000276:immunology; D015847:Interleukin-4 / Q000235:genetics / Q000276:immunology; D008168:Lung / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000009:adverse effects / Q000276:immunology
chemical_list: D004967:Estrogens; D018793:Interleukin-13; D015847:Interleukin-4; D010047:Ovalbumin