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

Xiang, Rong; Xu, Yu; Zhang, Wei; Kong, Yonggang; Tan, Lu; Chen, Shiming; Deng, Yuxiao; Tao, Zezhang

doi:10.1002/alr.22274

Cited by 19 publications

(14 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CD4 + IL-17 + Th17 cells were once discovered to induce autoimmune disorders [ 49 ]. Xiang et al’s study showed that sema3A which can exert immunoregulatory effect pulled down the raised percentage of CD4 + IL-17 + Th17 cells and inhibited allergic inflammation in OVA-induced mice [ 50 ]. Likewise, we found a high ratio of CD4 + IL-17 + Th17 cells to CD4 + T cells in RA mice, while CGA application lowered this ratio.…”

Section: Discussionmentioning

confidence: 99%

Chlorogenic acid ameliorated allergic rhinitis-related symptoms in mice by regulating Th17 cells

et al. 2020

View full text Add to dashboard Cite

Allergic Rhinitis (AR) is a non-infectious chronic inflammatory disease of nasal mucosa provoking Th17 response. Chlorogenic acid (CGA), one of the most abundant polyphenol compounds in various agricultural products, possess anti-viral, anti-inflammatory, and anti-bacterial properties. However, the effect of CGA on AR is unclear. Thus, our study explored the effect of CGA in modulating AR-related symptoms and immunoreaction especially Th17 response. AR mice were induced by ovalbumin (OVA) administration and further treated with CGA or dexamethasone. The frequencies of rubbing and sneezing of AR mice were recorded. Histopathological of nasal mucosa were conducted by hematoxylin-eosin staining and periodic acid-schiff staining. The serum and nasal mucosa levels of OVA-immunoglobulin (Ig)E, interferon (IFN)-γ, retinoic acid-associated nuclear orphan receptor (ROR)-γt, and interleukin (IL)-17A were measured by enzyme-linked immunosorbent assay, qRT-PCR, or western blot. The ratio of CD4+IL-17+Th17 cells to CD4+T cells in peripheral blood of AR mice was assessed by flow cytometer. CGA diminished the frequencies of rubbing and sneezing of AR mice in a concentration-dependent manner. CGA attenuated histopathological abnormalities and decreased goblet cell number in nasal mucosal of AR mice. CGA decreased the serum levels of OVA-IgE, ROR-γt, and IL-17A, while increasing the serum level of IFN-γ in AR mice. Meanwhile, CGA decreased the ratio of CD4+IL-17+Th17 cells to CD4+T cells in peripheral blood and the mRNA and protein levels of IL-17A and ROR-γt in AR mice. CGA ameliorated AR-related symptoms in mice by regulating Th17 cells, which could be a candidate for the treatment of AR.

show abstract

Section: Discussionmentioning

confidence: 99%

Chlorogenic acid ameliorated allergic rhinitis-related symptoms in mice by regulating Th17 cells

et al. 2020

View full text Add to dashboard Cite

show abstract

“…We assume that this effect is achieved by increasing local Treg functions, which subsequently reduces adaptive immune-mediated responses and pro-inflammatory cytokines. It is also possible that sema3A inhibits IL-17 production, indirectly leading to the reduced influx of neutrophils, although experimental proof for that is still required (29). So far there is no evidence for the presence of sema3A receptors on neutrophils and eosinophils.…”

Section: Discussionmentioning

confidence: 99%

Semaphorin 3A Is Effective in Reducing Both Inflammation and Angiogenesis in a Mouse Model of Bronchial Asthma

et al. 2019

View full text Add to dashboard Cite

Semaphorin 3A (sema3A) belongs to the sub-family of the immune semaphorins that function as regulators of immune-mediated inflammation. Sema3A is a membrane associated molecule on T regulatory cells and on B regulatory cells. Being transiently ligated to the cell surface of these cells it is suggested to be a useful marker for evaluating their functional status. In earlier studies, we found that reduced sema3A concentration in the serum of asthma patients as well as reduced expression by Treg cells correlates with asthma disease severity. Stimulation of Treg cells with recombinant sema3A induced a significant increase in FoxP3 and IL-10 expression. To find out if sema3A can be of benefit to asthma patients, we evaluated the effect of sema3A injection in a mouse model of asthma. BALB\c-mice were sensitized using ovalbumin (OVA) + adjuvant for 15 days followed by OVA aerosol inhalation over five consecutive days. Four hours following air ways sensitization on each of the above days- 15 of these mice were injected intraperitoneally with 50 μg per mouse of recombinant human sema3A-FR and the remaining 15 mice were injected with a similarly purified vehicle. Five days later the mice were sacrificed, broncheo-alveolar lavage (BAL) was collected and formalin-fixed lung biopsies taken and analyzed. In sema3A treated mice, only 20% of the bronchioles and arterioles were infiltrated by inflammatory cells as compared to 90% in the control group ( p = 0.0079). In addition, eosinophil infiltration was also significantly increased in the control group as compared with the sema3A treated mice. In sema3A treated mice we noticed only a small number of mononuclear and neutrophil cells in the BAL while in the control mice, the BAL was enriched with mononuclear and neutrophil cells. Finally, in the control mice, angiogenesis was significantly increased in comparison with sema3A treated mice as evidenced by the reduced concentration of microvessels in the lungs of sema3A treated mice. To conclude, we find that in this asthma model, sema3A functions as a potent suppressor of asthma related inflammation that has the potential to be further developed as a new therapeutic for the treatment of asthma.

show abstract

“…The AR murine model was established as previously described ( 17 ) with minor modifications (the mice were intranasally challenged on days 21–28). The miR-31 agomir was purchased from Guangzhou RiboBio Co., Ltd.…”

Section: Methodsmentioning

confidence: 99%

miR-31 attenuates murine allergic rhinitis by suppressing interleukin-13-induced nasal epithelial inflammatory responses

Zhou

Liu

et al. 2020

Mol Med Rep

Self Cite

View full text Add to dashboard Cite

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

Cited by 19 publications

References 32 publications

Chlorogenic acid ameliorated allergic rhinitis-related symptoms in mice by regulating Th17 cells

Chlorogenic acid ameliorated allergic rhinitis-related symptoms in mice by regulating Th17 cells

Semaphorin 3A Is Effective in Reducing Both Inflammation and Angiogenesis in a Mouse Model of Bronchial Asthma

miR-31 attenuates murine allergic rhinitis by suppressing interleukin-13-induced nasal epithelial inflammatory responses

Contact Info

Product

Resources

About