These results suggest that the suppression of IL-5 production through the suppression of IL-5 gene expression is one of the most important mechanisms by which glucocorticoids inhibit eosinophil functions in the treatment of atopic diseases, including bronchial asthma.
We studied the correlation between the eotaxin gene expression level in the material from nasal brushing and respiratory tests in asthma and COPD patients.
In sharp contrast, B7-H3 KO mice developed severe ovalbumin (OVA)-induced asthma with characteristic infiltrations of eosinophils in the lung, increased IL-5 and IL-13 in lavage fluid, and elevated IgE anti-OVA antibodies in the blood.
We examined TGFB1 SNPs in relation to asthma risk and degree of atopy among 546 case-parent triads, consisting of asthmatics aged 4-17 years and their parents in Mexico City.
These findings indicate that the IL-13 G+2044A is associated with asthma development and the IL-13 and IL-13Ralpha1 polymorphisms may interact to enhance IgE production.
Budesonide inhibited airway hyperreactivity, eosinophil counts in the lung and bronchoalveolar lavage (BAL) and CCL11, IL-13, and IL-23p19 release in the BAL of mice sensitized and challenged with <i>Af</i> (<i>p</i> < 0.05).
To assess the frequency of FLG mutations and the polymorphisms 590 C/T in the IL-4 gene, -1082A/G in the IL-10 gene and -1055C/T in the IL-13 gene in patients with AD and their correlations between severity of AD and asthma.
Areas covered: This review is based on recent English-language original articles in PubMed or Medline that reported significant clinical findings on the current status, therapeutic potential, and safety of biologics targeted at IL-4, IL-5, and IL-13 in the treatment of asthma together with the potential utility of simple reproducible non-invasive biomarkers to guide the effective use of biologic-based therapy that do not require direct sampling of the airways Expert commentary: The further development of reproducible and straightforward discriminatory non-invasive biomarkers may aid identification of those patients most likely to benefit from treatment with these interventions.
IL-5 levels were higher in induced sputum from patients with asthma and AR compared with nonatopic subjects (p = 0.020 and p = 0.032, respectively), but IFN-gamma levels showed no significant difference between the groups.
When compared to children with each CC of TLR4 polymorphism or TT of CD14 polymorphism or GG of IL13 polymorphism and no past history of bronchiolitis, children with CT or TT of TLR4 polymorphism and past history of bronchiolitis had 4.23 and 5.34 times higher risk to develop asthma, respectively; children with TT of CD14 polymorphism and past history of bronchiolitis had 3.57 and 7.22 times higher risk for asthma, respectively; children with GA or AA of IL-13 polymorphism and past history of bronchiolitis had 3.21 and 4.13 times higher risk for asthma, respectively.
CCR3 is the cognate receptor for major human eosinophil chemoattractants from the eotaxin family of proteins that are elevated in asthma and correlate with disease severity.
<b>Expert opinion</b>: IL-5 antagonism has paved the way for an additional personalized therapeutic opportunity for use in severe asthma with eosinophilic inflammation, though there is limited evidence on the long-term implications of suppressing/depleting eosinophils and the duration for which they should be administered.
These changes are mirrored in serum and should be considered in the light of the downmodulating role of CD26 in major chemokines related to the pathogenesis of asthma such as CCL11 (eotaxin), CCL5 (RANTES), and CXCL12a (SDF-1α).
Mouse models of asthma have shown that much of the airway dysfunction in these models can be generated by IL-13 stimulation of the airway epithelium alone.
Development of antagonistic antibody (Ab) against interleukin-4 receptor alpha (IL-4Rα) subunit of IL-4/IL-13 receptors is a promising therapeutic strategy for T helper 2 (T<sub>H</sub>2)-mediated allergic diseases such as asthma and atopic dermatitis.