Semaphorin 3A inhibits allergic inflammation by regulating immune responses in a mouse model of allergic rhinitis

2018 ◽  
Vol 9 (5) ◽  
pp. 528-537 ◽  
Author(s):  
Rong Xiang ◽  
Yu Xu ◽  
Wei Zhang ◽  
Yong‐Gang Kong ◽  
Lu Tan ◽  
...  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Gabija Drazdauskaitė ◽  
Janice A. Layhadi ◽  
Mohamed H. Shamji

Abstract Purpose of Review Allergic rhinitis (AR) is a chronic inflammatory immunoglobulin (Ig) E-mediated disease of the nasal mucosa that can be triggered by the inhalation of seasonal or perennial allergens. Typical symptoms include sneezing, rhinorrhea, nasal itching, nasal congestion and symptoms of allergic conjunctivitis. AR affects a quarter of the population in the United States of America and Europe. Recent Findings AR has been shown to reduce work productivity in 36–59% of the patients with 20% reporting deteriorated job attendance. Moreover, 42% of children with AR report reduced at-school productivity and lower grades. Most importantly, AR impacts the patient’s quality of life, due to sleep deprivation. However, a proportion of patients fails to respond to conventional medication and opts for the allergen immunotherapy (AIT), which currently is the only disease-modifying therapeutic option. AIT can be administered by either subcutaneous (SCIT) or sublingual (SLIT) route. Both routes of administration are safe, effective, and can lead to tolerance lasting years after treatment cessation. Both innate and adaptive immune responses that contribute to allergic inflammation are suppressed by AIT. Innate responses are ameliorated by reducing local mast cell, basophil, eosinophil, and circulating group 2 innate lymphoid cell frequencies which is accompanied by decreased basophil sensitivity. Induction of allergen-specific blocking antibodies, immunosuppressive cytokines, and regulatory T and B cell phenotypes are key pro-tolerogenic adaptive immune responses. Conclusion A comprehensive understanding of these mechanisms is necessary for optimal selection of AIT-responsive patients and monitoring treatment efficacy. Moreover, it could inspire novel and more efficient AIT approaches.


2015 ◽  
Vol 53 (4) ◽  
pp. 353-358 ◽  
Author(s):  
B.Y. KIm ◽  
H.R. Park ◽  
H.G. Jeong ◽  
S.W. Kim

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Yunxiu Wang ◽  
Zhiwei Cao ◽  
He Zhao ◽  
Yaoyao Ren ◽  
Liying Hao ◽  
...  

Purpose. Bisphenol A (BPA) is found in many plastic products and is thus a common environmental endocrine disruptor. Plastic-related health problems, including allergic diseases, are attracting increasing attention. However, few experimental studies have explored the effect of BPA on allergic rhinitis (AR). We explore whether BPA was directly related to the allergic inflammation induced by ovalbumin (OVA) in AR mice. Methods. We first constructed OVA-induced mouse model, and after BPA administration, we evaluated nasal symptoms and measured the serum OVA-specific IgE levels by ELISA. Th2 and Treg-related cytokines of nasal mucosa were measured by cytometric bead array. Th2 and Treg-specific transcription factor levels were assayed by PCR. The proportions of CD3+CD4+IL-4+Th2 and CD4+Helios+Foxp3+ T cells (Tregs) in spleen tissue were determined by flow cytometry. Results. Compared to OVA-only-induced mice, BPA addition increased nasal symptoms and serum OVA-specific IgE levels. OVA and BPA coexposure significantly increased IL-4 and IL-13 protein levels compared to those after OVA exposure alone. BPA plus OVA tended to decrease the IL-10 protein levels compared to those after OVA alone. Coexposure to OVA and BPA significantly increased the GATA-3-encoding mRNA level, and decreased the levels of mRNAs encoding Foxp3 and Helios, compared to those after OVA exposure alone. BPA increased the Th2 cell proportion, and decreased that of Tregs, compared to the levels with OVA alone. Conclusion. BPA exerted negative effects by exacerbating AR allergic symptoms, increasing serum OVA-specific IgE levels, and compromising Th2 and Treg responses.


2016 ◽  
Vol 273 (11) ◽  
pp. 3783-3788 ◽  
Author(s):  
Mei-Jun Liang ◽  
Qing-Ling Fu ◽  
Hong-Yan Jiang ◽  
Feng-Hong Chen ◽  
Dong Chen ◽  
...  

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