Significant reduction in the IL-17 gene expression following administration of synbiotic versus placebo shows the importance of synbiotic in control of the immunopathogenesis of AR.
We sought to obtain mechanistic insight into how IL-17A and IL-13 regulate the epithelial production of eotaxin-3 representing eosinophilic inflammation in AR.
Moreover, HE lowered the levels of serum IgE and histamine and inhibited IL-4 and IL-17 levels from AR mice but raised IL-2 and IFN-γ levels in AR-induced nasal lavage fluid.
Local production of IL-22 and IL-17A in PAR patients and healthy controls' nasal mucosa was examined by immunohistochemistry (IHC) and real-time polymerase chain reaction (RT-PCR) techniques.
Compared with the control group, interferon-γ (IFN-γ) was significantly down-regulated, while IL-4, IL-17, and IL-9 were significantly elevated in the AR model group.
The results of the present study suggested that patients with AR have raised mitochondrial ROS levels, which may upregulate the expression of IL-1β, affecting IL-17-production and serving a role in the pathogenesis of AR.
The objective was to evaluate the association between IL-17Ars2275913 (-197G>A) polymorphism and post-bronchiolitis asthma and/or allergic rhinitis in a prospective 11-13 years post-bronchiolitis follow-up.
Recombinant IL‑37 (rIL‑37) inhibited the production of IL‑1p and IL‑6, and enhanced the production of IL‑27 in PBMCs from the patients with AR and the control individuals. rIL‑37 also markedly decreased the expression of IL‑17 by CD4+ T cells in the patients with AR and controls.
Compared with the normal controls, neonatal offspring of Der p 1-stimulated female mice (AR offspring) showed the elevation of interleukin (IL)-4 (P<0.01) and IL-17 (P<0.01), the submission of IL-10 (P<0.01) in spleen homogenates.
The suppression of nasal inflammation due of IL-17A deficiency in allergic rhinitis is partly responsible for the regulation of CCL7 secretion and eosinophil infiltration, which may be regulated via the CCL7/CCR3 pathway.
AR mice shown significantly increased Th2 and Th17 cell ratio in spleen, IL-17 level in serum, IL-5 and IL-13 levels in NALF but a lower number of IL-33-positive epithelial cells and Th1 response (Th1 and Tbet<sup>+</sup>Th1 cell ratio in the spleen and serum IFN-γ level) than the control mice.1,25-(OH)<sub>2</sub>D<sub>3</sub> treatment significantly decreased the number of sneezing, nasal rubbing, OVA-sIgE and IL-17 in serum, IL-5 and IL-13 levels in NALF, Th17 cell ratio in the spleen and the histological of nasal mucosal but increased the number of IL-33-positive epithelial cells in AR mice.
The SIT effect was evaluated by assessing clinical symptoms. mRNA levels of Th17 specific genes (IL17 and RORC) were increased in SIT-untreated AR versus controls, and decreased following SIT treatment.
Our findings preliminarily indicate IL17A and IL17F SNPs, and some intergenic variants have the potential association with AR and comorbid asthma in Chinese population.
Two new T cell subsets may be involved in allergic rhinitis (AR) pathogenesis: Th17 and T regulatory cells, mainly producing IL-17 and TGF-beta respectively.