Quantitative PCR (qPCR) and enzyme-linked immunosorbent assay (ELISA) were performed to detect the expression of interleukin 27 (IL-27) and Th2 cytokines (IL-4, IL-5, IL-13) from 22 patients diagnosed with AR and 20 normal controls.
PGD<sub>2</sub> -CRTH2 and cysLTs-CysLT1 axes may activate tissue-resident ILC2s to produce Th2 cytokines, IL-5 and IL-13, leading to the development of allergic inflammation in 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.
Compared with the GFP-DC/AR group, mice in the Der p1-DC/AR group showed an ameliorated allergic response, a significant decrease in the levels of serum IgE, IgG1, and histamine, and a decrease in the expression of IL-4 and IL-13 mRNA and protein in the nasal mucosa.
In mice with AR, AST2017-01 and chrysophanol markedly decreased number of rubs, IgE, histamine, thymic stromal lymphopoietin, tumor necrosis factor-α, interleukin (IL)-1β, IL-4, IL-5, and IL-13 in serum or nasal mucosa tissues.
In addition, the expression levels of inflammatory factors were higher in the blood of mice with AR compared with the control group, while miR-let-7e overexpression inhibited these levels in AR mice and IL-13-stimulated NECs.
The frequencies of sneezing and scratching, as well as the levels of IgE, IL-4, and IL-13, in the serum were higher in the AR group than in the control group (p<0.01), whereas all these parameters were decreased significantly after HRS treatment (p<0.05).
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.
After adjustments, the presence of the IL13 rs20541A- allele (OR 3.06, 95% CI 1.42-6.58, p = 0.004) or multisensitization (adjusted OR 4.59, 95% CI 1.48-14.26, p = 0.008) was associated with AR/AC asthma.
As IL13, a pleiotropic cytokine, may be important in conferring susceptibility to AR, the aim of the present work was to assess the relationship between a CpG island methylation status at the upstream of IL13 gene and house dust mite (HDM)-sensitized AR in Han Chinese subjects.
miR-143 inhibits interleukin-13-induced inflammatory cytokine and mucus production in nasal epithelial cells from allergic rhinitis patients by targeting IL13Rα1.
The risk of current AR also increased in subjects with GA or AA at nucleotide 2044 in IL13 who had been exposed to mold in the home during infancy (adjusted odds ratio, 3.27; 95% CI, 1.75-6.11) compared with subjects who had GG at this position and had not been exposed to mold (adjusted odds ratio, 3.27; 95% CI, 1.75-6.11).
The IL-13R A(1) +1398 A/G polymorphism does not contribute to asthma or allergic rhinitis susceptibility, yet serum IL-13 can be used as a marker in atopic diseases and to differentiate between atopic and non-atopic asthma.
However, a recent meta-analysis using data from these 6 studies has shown that the A allele of IL13 SNP rs20541 was associated with an increased risk of allergic rhinitis, whereas no such relationship existed between IL13 SNP rs1800925 and allergic rhinitis.
A model with rs1058240, rs379568, and rs4143094 (GATA3) and rs1800925 (IL13) and their interactions was selected to predict rhinitis and positive SPT responses. rs1058240 was associated with rhinitis and allergic rhinitis (P < .05), and the gene-gene interaction rs1058240:rs1800925 was associated with rhinitis (P = .043).
Our results suggest that the IL-13 exon 4 G2044A polymorphism confers susceptibility to the development of allergic rhinitis in Koreans, whereas the IL-4Ralpha Gln551Arg polymorphism is not related to allergic rhinitis.
Environmental antigen-induced IL-13 responses are elevated among subjects with allergic rhinitis, are independent of IL-4, and are inhibited by endogenous IFN-gamma synthesis.