We examined the effects of sex hormones on the functions of eosinophils. Treatment of eosinophils with beta-estradiol significantly enhanced the eosinophil adhesion to human mucosal microvascular endothelial cells (HMMEC), and eosinophils stimulated by a combination of beta-estradiol and progesterone showed significant induced degranulation. On the other hand, testosterone significantly reduced the eosinophil adhesion to HMMEC and eosinophil viability. The experiments from the series of studies might provide a partial explanation for the aggravation of asthma and some forms of rhinitis that occurs during pregnancy.

Background: Hyperreactivity of the nasal mucosa is a characteristic of nasal allergy. During pregnancy, aggravation of nasal allergic symptoms is occasionally observed in subjects with nasal allergy. Methods: Using the reverse transcription-polymerase chain reaction and Southern blot hybridization method, we investigated histamine H1 receptor mRNA (H1R mRNA) expressions in specimens of nasal epithelial layer obtained by scraping, as well as cultured human nasal epithelial cells (HNECs) and human mucosal microvascular endothelial cells (HMMECs). We compared the expressions on the specimens from patients with nasal allergy with those with nonallergic rhinitis or those from normal volunteers. In addition, we investigated the effects of female hormones on the H1R mRNA expressions in HNECs and HMMECs. Results: H1R mRNA was detected in scraped specimens of nasal epithelial layer, as well as in HNECs and HMMECs. The mRNA expressions in nasal mucosal scraped specimens of epithelial layers and HNECs were more marked in patients with nasal allergy than in the other two groups. In addition, the present study demonstrates that the female hormones β-estradiol and progesterone significantly increase the expressions of H1R mRNA on HNECs and HMMECs. Conclusion: The increase of the expressions of H1R mRNA may explain, in part, the nasal hyperreactivity to histamine observed in patients with nasal allergy. It has also been suggested that sex hormones are related to the preponderance of females in the incidence of allergic rhinitis after puberty, and that they are related, at least partially, to the aggravation of the nasal hyperreactivity symptoms during pregnancy through the enhanced expression of H1R mRNA on HNECs and HMMECs.

These results strongly suggest that DEP accelerates the inflammatory change by not only directly upregulating H1R expression but also increasing histamine-induced IL-8 and GM-CSF production.

Diesel exhaust particulates (DEP) are a common air pollutant from diesel-engine-powered car exhaust and are thought to cause chronic airway diseases. On the other hand, eosinophils are major components of allergic inflammatory disorders such as asthma, nasal allergy and atopic dermatitis. We examined the effects of DEP and DEP extract (extract of polyaromatic hydrocarbons) on eosinophil adhesion, survival rate and degranulation. Eosinophils, human mucosal microvascular endothelial cells (HMMECs) and human nasal epithelial cells (HNECs) were preincubated in the presence or absence of DEP and DEP extract. ³⁵S-labeled eosinophils were allowed to adhere to monolayers of HMMECs and HNECs. After washing, ³⁵S radioactivity was determined and numbers of adherent eosinophils were calculated using each standard curve. The effects of DEP and DEP extract on eosinophil survival rate and degranulation were also determined. Although neither DEP nor DEP extract affected the adhesiveness of HMMECs and HNECs to eosinophils, 5 ng/ml of DEP extract and 50 ng/ml of DEP extract each significancy increased eosinophil adhesiveness to HNECs (134 ± 9 and 143 ± 8%, respectively; p < 0.01 vs. control), but neither effected eosinophil adhesiveness to HMMECs. DEP extract also induced eosinophil degranulation without changing the eosinophil survival rate. Given that eosinophil-derived lipid mediators and toxic proteins play important roles in the development of nasal allergy, the above findings strongly suggest that DEP plays an important role in promoting the nasal hypersensitivity induced by enhanced eosinophil infiltration of epithelium and eosinophil degranulation.

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