These findings are compatible with the hypothesis that IL-10 mRNA is expressed in both macrophages and T lymphocytes in the airway in asthma and that IL-10 mRNA expression is induced from T lymphocytes in response to allergen.
As a prototype for both cytokines, work relating to an interleukin (IL)-4 promoter polymorphism and an IL-10 promoter polymorphism will be reviewed as providing a potential molecular mechanism for dysregulation of these cytokine genes in asthma.
We investigated the hypothesis that polymorphic nucleotides within the IL-10 and TGF-beta gene promoters would link to the expression of allergies and asthma.
Our results support the hypothesis that IL-10 overexpression may counterbalance the effects of proinflammatory cytokines and mitigate the inflammatory reaction found in gut mucosa of subjects with asthma.
These are the IL10 -592C>A SNP in the interleukin 10 gene (p=0.036 for eosinophil cell counts), the 4124T>C SNP in EDN1 (p=0.044 for asthma), the 3391C>T SNP in NOS1 with eosinophil cell counts (p=0.0086), and the 5266C>T polymorphism, also in the NOS1 gene, for high IgE levels (p=0.022).
The distribution of CC homozygotes in the IL-10 gene was significantly lower in asthma patients than in controls (P=0.013, OR=3.599, 95% CI=1.240 approximately 10.441).
The aim of this study was to test whether the polymorphisms of the promoter region and exon 5 of the IL-1 gene, intron 2 of the IL-1Ra gene, and -627 nucleotide (C/A) of the IL-10 gene could be genetic markers for the susceptibility of bronchial asthma.
Decreased LPS-induced IL-12(p70) and IL-10 responses were associated with the TLR4 (Asp299Gly) polymorphism and independently with asthma, especially atopic asthma.
At least one positive SNP with a TDT of p < 0.05 for asthma or total IgE and calcidiol or calcitriol was seen in IL10, GC, IL12B, CYP2R1, IL4R, and CYP24A1.
Although IL-10-producing (IL-10+) T cells are detectable in the peripheral blood, their significance in the pathophysiology of asthma remains uncertain.
When phenotypes of individuals with a physician's diagnosis of asthma were excluded, IL10 SNPs remained significantly associated, suggesting that the association with airflow obstruction was independent of an association with asthma.
Our findings suggest that dust mite allergen levels modify the effect of IL10 SNPs on allergy and asthma exacerbations and may partly explain conflicting findings in this field.
Our findings suggest that dust mite allergen levels modify the effect of IL10 SNPs on allergy and asthma exacerbations and may partly explain conflicting findings in this field.
IL-10(-1082(G-->A)) G/G and TNF-alpha-308(G-->A) G/G may be a contributing factor in susceptibility as well as severity of asthma among Egyptian children.
IL-10(-1082(G-->A)) G/G and TNF-alpha-308(G-->A) G/G may be a contributing factor in susceptibility as well as severity of asthma among Egyptian children.
The plasma IL-10 and IL-12 levels of the patients in the asthma group were significantly lower than those of the healthy adults in the control group (p < 0.05), while IgE gave the opposite result (p < 0.0001).