The association between allergic rhinitis and Polymorphism of Toll like receptors 2 & 4 genes

Background: Allergic rhinitis is atopic disorder, 10% to 25% of the population worldwide are suffering from it, The prevalence is increasing during the last 10 years. Objectives: To study the relationship among polymorphism of single nucleotide in TLR2 and TLR4 genes and the risk of allergic rhinitis disease. Methodology: This study was done on 60 patients suffering from allergic rhinitis and 30 healthy subjects as a control group from April 2019 to March 2020. The patients were collected from Otorhinolaryngology Department of Benha University Hospital. Test of Skin prick (SPT) was done to assess atopic state. Blood samples were collected to detect TLR gene polymorphism by Polymerase chain reaction-Restriction Fragment Length Polymorphism (PCR-RFLP). Results: The genotypic frequencies of TLR2 Arg753Gln showed increased frequency of the homozygous (GG) genotype among the controls (80%) more than the allergic rhinitis patients (30%). The heterozygous (AG) genotype was increased among the allergic rhinitis patients (62.5%) more than in the healthy group (15%) with OR =9.4, 95% CI (2.4-37.7) and significant P-value. Also, the homozygous mutant (AA) genotype has more trend in the patients (7.5%) than in the control subjects (5%), with OR = 0. 6, 95% CI (0.1-6.7) and non-significant P-value. The genotypic frequencies Statistical data in TLR4 Asp299Gly revealed that the homozygous (AA) genotype has more frequency in the controls (70%) than the allergic rhinitis patients (20%). The heterozygous (AG) genotype was more prevalent among the allergic rhinitis patients (65%) than the controls (30%) with OR =4.3, 95% CI (1.4-13.8) and significant P-value. Conclusion: GG genotype of TLR2 and AA genotype of TLR4 are least affected by allergic rhinitis disease and the major allele in both gene is protective against the disease.

Features of Neutrophils From Atopic and Non-Atopic Elite Endurance Runners

We collected peripheral blood from thirty-nine elite male endurance runners at rest (24 hours after the last exercise session) and used the Allergy Questionnaire for Athletes score and plasma specific IgE level to separate them into atopic and non-atopic athletes. Neutrophils obtained from atopic and non-atopic athletes were subsequently stimulated in vitro with fMLP (N-formyl-methionyl-leucyl-phenylalanine), LPS (lipopolysaccharide), or PMA (phorbol 12-myristate 13-acetate). Neutrophils from non-atopic runners responded appropriately to LPS, as evidenced by the production of pro (IL-8, TNF-α, and IL-6) and anti-inflammatory (IL-10) cytokines. Neutrophils from atopic elite runners exhibited lower responses to LPS stimulus as indicated by no increase in IL-1β, TNF-α, and IL-6 production. Neutrophils from non-atopic and atopic runners responded similarly to fMLP stimulation, indicating that migration function remained unaltered. Both groups were unresponsive to PMA induced reactive oxygen species (ROS) production. Training hours and training volume were not associated with neutrophil IgE receptor gene expression or any evaluated neutrophil function. Since non-atopic runners normally responded to LPS stimulation, the reduced neutrophil response to the stimuli was most likely due to the atopic state and not exercise training. The findings reported are of clinical relevance because atopic runners exhibit a constant decline in competition performance and are more susceptible to invading microorganisms.