Introduction Postorgasmic illness syndrome (POIS) is a rarely described syndrome characterized by transient flu-like symptoms and cognition disorders. Recent studies suggest that immunogenic reactivity to autologous semen is the underlying mechanism in POIS. However, there are no data published on immunoglobulin E (IgE)-mediated allergy to autologous semen in men without POIS. Aim The purpose of the current work was to characterize the first diagnosed POIS patient in China and to study the allergic response of autologous semen in the affected patient and in three healthy males. Methods Specific IgE was tested with seminal fluid and common perennial aeroallergens in vitro. Skin prick tests and intracutaneous tests with autologous diluted semen were performed in the patient and three healthy donors. The pattern of IgE reactivity to patient's semen was identified using immunoblotting and ELISA. Main Outcome Measure Clinical features of POIS, skin reactions with autologous diluted seminal fluid, and the IgE reactivity patterns of immunoblotting and ELISA in vitro. Results A patient was diagnosed with POIS. The patient complained of lifelong premature ejaculation symptoms and allergic rhinitis. Routine laboratory and hormonal assessments were generally within normal range. The patient had a positive skin test with his own semen. Three healthy donors also showed positive skin tests. No semen-specific IgE to autologous semen was detected in the serum of the affected patient or healthy males. Conclusions This is the first report of a man with POIS in China. He had positive skin reactions after injection of autologous seminal fluid but no detectable serum concentrations of specific IgE antibodies. IgE-mediated semen allergy in men may not be the potential mechanism of POIS.

Objective. This study is aimed at investigating the role of substance P (SP) in the development of asthma. Methods. The Gene Expression Omnibus (GEO) database was used to characterize SP expression in allergic rhinitis (AR) and asthma. Peripheral blood was collected from patients with asthma or AR. The expression of relevant cytokines and neuropeptides was measured. Enzyme-linked immunosorbent assay (ELISA) was also performed. The mast cell line LAD2 and the lung bronchial epithelial cell line BEAS-2B were treated with different concentrations of SP concentration. Then, the qRT-PCR method was used to determine the mRNA expression. Furthermore, p38 and p65 and their associated phosphorylated proteins (p-p38 and p-p65) were further validated by western blotting. Result. Clinical and GSE75011 data analysis suggested that MyD88 expression was upregulated in AR and asthma. Through the gene set variation analysis (GSVA), MyD88-related pathways were noticed and further investigated. ELISA results suggested that the SP expression was significantly increased in AR and asthma and IL-10 expression was decreased, whereas the expression of IL-6, IL-17A, IL-23, and TGF-β expressions increased. The mast cell line LAD2 was treated with different SP concentrations, and ELISA results showed that the expression of IL-6, IL-17A, IL-23, and TGF-β in the cell supernatant gradually increased with increasing SP concentrations, whereas that of IL-10 decreased. The lung bronchial epithelial cell line BEAS-2B was treated with different SP concentrations, and the expression of myeloid differentiation factor 88 (MyD88) and its related proteins was elevated. The expression of p38 and p-p38 proteins was elevated after SP treatment, and their expression levels elevated as SP concentrations increased. Finally, MyD88 expression at the single-cell level was also demonstrated. Conclusion. SP may affect the cytokine expression through the MyD88 pathway, thereby influencing Th17/Treg differentiation and eventually participating in the pathological process of asthma and AR. There are many pathological similarities between allergic rhinitis (AR) and bronchial asthma. In the present study, SP was found to possibly activate downstream inflammatory signaling pathways via MyD88, thereby affecting Th17/Treg differentiation and ultimately participating in the pathological process of asthma and AR.