Abstract
Innate immunity plays a central role in the pathogenesis of severe asthma, and it is closely linked to elevated IgE and Toll-like receptor 4 (TLR-4) levels. However, there is a scarcity of information about the association of the TLR-4 receptor polymorphism in the pathogenesis of severe asthma. This study highlights the level of gene expression of different alleles in asthmatic patients compared to healthy control individuals. This was a randomized control trial, which included 150 patients with asthma (with high serum levels of IgE) with a matching 150 healthy control individuals. Participants had a series of blood tests to measure various immune parameters: interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor (TNF), intercellular adhesion molecule-1 (ICAM1) and detect allele type and gene expression of the TLR-4 gene. Patients with asthma had significantly higher levels of IL-8 when compared to the healthy control participants. In addition, in the rs91 genotyping, there were significant differences in the levels of IL-8 and TNF between CC and TT genotyping. While in rs90 TLR-4, TNF levels were significantly higher in AA vs. AG and GG genotypes among the asthmatic patients when compared to the control group. The results showed that in TLR-4, rs4986791 were significantly associated with asthma risk. Polymorphisms in TLRs play essential roles in asthma.
Highlights
Bronchitis and reverse airway obstruction are among the most important features of asthma, and it has significantly increased in recent decades [1]
There was a significant increase in the plasma levels of interleukin-8 (IL-8) and tumor necrosis factor (TNF) in the CC genotype, while the CT genotype showed a smaller rise in the IL-8 levels, but still significant (P
There was a significant increase in the plasma levels of IL-8, IL-1, and TNF in the GG genotype, while the AA genotype showed only a smaller rise in the IL-1 levels, but still significant (P
Summary
Bronchitis and reverse airway obstruction are among the most important features of asthma, and it has significantly increased in recent decades [1]. The link between asthma and innate immunity has been previously shown by many studies, with evidence that the response to antivirals decreases bronchial cells in asthma patients, as well as increases the expression of receptors in severe asthma. This indicates that innate immunity has active participation in the exacerbation of asthma, and innate immunity represents the first line of defense against microbes. The Toll-like receptor (TLR) family comprises receptors belonging to innate immunity with the mission of identifying microbes and activating immunity with both fungal and adaptive types by different cells in the airway, including fat cells, macrophages, and epithelial cells. Activation of innate immunity, especially TLR-4 receptors, is dependent on air pollutants, such as ozone, CO2, and N2
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