Increased Risk Of Allergic Rhinitis Research Articles

Association of ANRIL Gene Single-Nucleotide Polymorphisms With Allergic Rhinitis in Kurdish Population From Kermanshah, Iran.

Allergic rhinitis (AR) is the most common inflammatory disorder of the upper airway caused by aberrant immune responses to allergens in genetically predisposed individuals. Recently, the long noncoding RNA (lncRNA) antisense noncoding RNA in the INK4 locus (ANRIL) has been identified as a novel genetic factor associated with increased AR risk. This study aimed to evaluate the potential correlation of ANRIL gene single nucleotide polymorphisms (SNPs) with AR risk in the Kurdish population of Kermanshah, Iran. In this case-control study, 130 AR patients and 130 healthy controls were recruited to genotype for two SNPs of the ANRIL gene (rs1333048 and rs10757278) using the Tetra-primer amplification refractory mutation system polymerase chain reaction (T-ARMS-PCR) method. Our results showed no significant difference for the alleles and genotypes frequency distribution of lncRNA ANRIL SNPs (rs1333048 and rs10757278) between AR patients and healthy controls (p > 0.05). Additionally, the dominant, additive and recessive genetic models of both SNPs were not associated with altered susceptibility to AR risk (p > 0.05). The results demonstrated that the ANRIL gene rs1333048 and rs10757278 polymorphisms might not be associated with susceptibility to AR in the Kurdish population of Kermanshah, Iran.

Effects of early life exposure to home environmental factors on childhood allergic rhinitis: Modifications by outdoor air pollution and temperature.

There is growing evidence that allergic rhinitis (AR) is associated with indoor environmental factors, but their role in childhood AR during early life remains unclear. To investigate the association of preconceptional, prenatal, early postnatal, and current exposure to home environmental factors with childhood AR, and to further explore whether this association can be interacted by outdoor air pollution and temperature. A retrospective cohort study of 8689 preschool children was conducted during 2019-2020 in Changsha, China. A standard questionnaire was used to collect data on each family's health outcomes and home environments. We considered home environmental exposures during one year before conception, pregnancy, first year of life, and past year. Associations of indoor air pollution and allergens with AR were assessed by multiple logistic regression models. Pre-birth exposure to indoor air pollution emitted by new furniture or redecoration and dampness related allergen derived from mold/damp stains and mold/damp clothes or bedding during 1 year before conception and pregnancy was significantly associated with increased AR, with adjusted ORs (95% CI) ranging from 1.35 (1.05-1.75) to 1.87 (1.55-2.27). Childhood AR was also significantly related with post-birth exposure to dampness related indoor allergen including mold/damp stains and mold/damp clothes or bedding in first year and past year and pollen allergen including total and nonflowing plants in past year, with a range of ORs (95% CI) from 1.20 (1.01-1.42) to 1.79 (1.42-2.27). We identified that pre-birth, particularly in utero exposure to both indoor air pollution from renovation and dampness related allergens, played a key role in AR development compared to post-birth exposures, and accumulative effect was observed with the highest risk of AR. High exposure to traffic-related air pollution (TRAP) including outdoor PM2.5, NO2, CO, and O3, as well as living near traffic road not only significantly increased adverse effect of home environmental factors but also decreased protective effect of household dogs on childhood AR. Early life exposure to low temperature in pregnancy and high temperature in first year significantly increased AR risk of home environmental exposure. Sensitivity analysis indicated that some sub-groups were more susceptible to AR risk of home environmental exposure. Our study suggests that pre-birth exposure to home environmental factors played an important role in AR development and this effect can be interacted by TRAP and temperature, which supports a hypothesis of "(pre)fetal origin of childhood AR".

Sensitization to Airborne Fungal Allergens Associates with Asthma and Allergic Rhinitis Presentation and Severity in the Singaporean/Malaysian Population

Fungal spores and conidia are the major components of total airspora in the tropical Asia environment, and their sensitization patterns are often associated with allergic diseases such as asthma, allergic rhinitis (AR), and atopic dermatitis. Hence, we recruited a cross-sectional cohort of 9223 Singapore/Malaysia Chinese adults and assessed their sensitization against Curvularia lunata allergen using the skin prick test approach. A subset of this cohort (n = 254) was also screened for specific Immunoglobulin E (sIgE) titers against a panel of 11 fungal allergens. We found significant association of Curvularia lunata sensitization with the risk of asthma (OR = 1.66, 95% CI: 1.17–2.33; p = 0.00391) and AR (OR = 1.69, 95% CI: 1.18–2.41; p = 0.00396). Among asthmatic patients (n = 1680), Curvularia lunata sensitization also increased frequencies of wheezing symptoms (OR = 1.81, 95% CI: 1.05–2.96; p = 0.0239), general practitioner/specialist visits (OR = 2.37, 95% CI: 1.13–4.61; p = 0.0157), and other asthma-related exacerbation events (OR = 2.14, 95% CI: 1.04–4.10; p = 0.0289). In our serum cohort, sensitization to Aspergillus spp. was the most common fungal sensitization, with 23.6% (n = 60) had a class 3 and above sensitization (positive sensitization; sIgE titers of > 3.5 kU/L) against this allergen. Increasing sIgE titer against Aspergillus spp. was also correlated with increased AR risk and AR-related symptoms. In conclusion, our findings emphasize an important role of fungal sensitization in the manifestations of asthma and AR in the Southeast Asian Chinese population.

Interaction between early-life pet exposure and methylation pattern of ADAM33 on allergic rhinitis among children aged 3\u20136\xa0years\xa0in China

BackgroundRecent research has pointed out the important roles of epigenetic modifications in the development and persistence of allergic rhinitis (AR), especially in relation to DNA methylation of disease-associated genes. We investigated whether AR susceptibility genes were epigenetically regulated, and whether methylation modulation of these genes in response to early-life environment could be a molecular mechanism underlying the risk for AR onset in a cohort of children aged 3–6 years in China.MethodsPeripheral blood mononuclear cell (PBMC) samples were collected from 130 children patients, aged 3–6 years and diagnosed with AR; and 154 matched controls to detect promoter methylation in 25 AR susceptibility genes with the MethylTarget approach. Methylation levels were compared for each CpG site, each amplified region, and each gene. In addition, the relationship among DNA methylation, early-life environmental risk factors and AR onset were assessed.ResultsMaternal allergic history (P = 0.0390) and pet exposure (P = 0.0339) were significantly associated with increased AR risk. Differential methylation analyses were successfully performed for 507 CpG sites, 34 amplified regions and 17 genes and significant hypomethylation was observed in the promoter region of ADAM33 in AR patients [multiple test-corrected (FDR) P-value < 0.05]. Spearman correlation analysis revealed that the hypomethylation of ADAM33 was significantly associated with higher eosinophil counts (Spearman’s ρ: − 0.187, P-value = 0.037). According to the results of the multiple regression analysis, after adjusting for cofounders, the interaction of early-life pet exposure with methylation level of ADAM33 increased the risk for AR onset 1.423 times more in children (95% CI = 0.0290–4.109, P-value = 0.005).ConclusionThis study provides evidence that early-life pet exposure and low methylation level of ADAM33 increase AR risk in children, and the interaction between pet exposure and methylation level of ADAM33 may play an important role in the development of AR.

Associations between air pollution and outpatient visits for allergic rhinitis in Xinxiang, China.

Several epidemiological studies have investigated the adverse health effects of air pollution, but studies reporting its effects on allergic rhinitis (AR) are limited, especially in developing countries having the most severe pollution. Limited studies have been conducted in China, but their results were inconsistent. So, we conducted a time-series study to evaluate the acute effect of six air pollutants (fine particulate matter [PM2.5], particulate matter with diameter less than 10μm [PM10], sulfur dioxide [SO2], nitrogen dioxide [NO2], ozone [O3], and carbon monoxide [CO]) on hospital outpatient visits for AR in Xinxiang, China from January 1, 2015, to December 31, 2018. An over-dispersed Poisson generalized additive model adjusting for weather conditions, long-term trends, and day of the week was used. In total, 14,965 AR outpatient records were collected during the study period. Results found that each 10μg/m3 increase in PM2.5, PM10, SO2, NO2, O3, and CO corresponded to 0.70% (95% confidence interval 0.00-1.41%), 0.79% (0.35-1.23%), 3.43% (1.47-5.39%), 4.54% (3.01-6.08%), 0.97% (-0.11-2.05%), and 0.07% (0.02-0.12%) increments in AR outpatients on the current day, respectively. In the stratification analyses, statistically stronger associations were observed with PM2.5, PM10, SO2, NO2, and CO for AR outpatients <15years of age than in those 15-65 and ≥ 65years of age, whereas the opposite result was found with O3. Associations between PM10, SO2, NO2, O3, and AR outpatients were higher in the warm season than those in the cool season. This study suggests that exposure to PM2.5, PM10, SO2, NO2, and CO was associated with increased AR risk and children younger than 15years might be more vulnerable.

Angiotensin-converting enzyme insertion/deletion polymorphism associated with allergic rhinitis susceptibility: Evidence from 1410 subjects

Whether the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene increases susceptibility to allergic rhinitis (AR) is still undetermined. Therefore, this meta-analysis was performed to systematically assess the possible association between them. The OVID, Medline, Embase, Web of Science, CNKI and Wangfang databases were searched to identify the eligible studies focusing on the association between ACE I/D polymorphism and susceptibility to AR. A total of 1410 subjects from six studies were subjected to meta-analysis. In the overall analysis, ACE I/D polymorphism had a statistically significant association with increased AR risk under all genetic models (p<0.05). In the subgroup analysis by ethnicity, significant elevated AR risks were associated with ACE I/D polymorphism in Asians under all genetic models (p<0.05) and in Caucasians under under allele contrast, homozygous comparison and recessive models (p<0.05). In the subgroup analysis by age, ACE I/D polymorphism was associated with significant elevated risks of AR in adults (p<0.05) but not in children (p>0.05) under all genetic models. The ACE I/D polymorphism may be a risk factor for AR and studies with large sample size and representative population are warranted to verify this finding.

Association of interleukin-13 SNP rs20541 with allergic rhinitis risk: A meta-analysis

Studies investigating the association between interleukin-13 (IL-13) single nucleotide polymorphism (SNP) rs20541 and allergic rhinitis (AR) risk have reported conflicting results. The aim of the present study was to conduct a meta-analysis assessing the possible association of IL-13 SNP rs20541 with AR risk. Eight studies were included in the present meta-analysis (2153 cases and 3931 controls). The combined results based on all studies showed that IL-13 SNP rs20541 was associated with increased AR risk (Gln versus Arg: odds ratio (OR)=1.18, 95% confidence interval (CI)=1.08–1.30; Gln/Gln versus Arg/Arg: OR=1.52, 95% CI=1.20–1.92; Arg/Gln+Gln/Gln versus Arg/Arg: OR=1.19, 95% CI=1.06–1.33; Gln/Gln versus Arg/Gln+Arg/Arg: OR=1.42, 95% CI=1.13–1.79). When stratifying for race, IL-13 SNP rs20541 exhibited increased AR risk in Asians (Gln versus Arg: OR=1.20, 95% CI=1.06–1.36; Gln/Gln versus Arg/Arg: OR=1.57, 95% CI=1.17–2.12; Arg/Gln+Gln/Gln versus Arg/Arg: OR=1.22, 95% CI=1.04–1.44; Gln/Gln versus Arg/Gln+Arg/Arg: OR=1.45, 95% CI=1.09–1.93), while no significant association was detected in Caucasians (Gln versus Arg: OR=1.28, 95% CI=0.93~1.78; Gln/Gln versus Arg/Arg: OR=1.42, 95% CI=0.96–2.11; Arg/Gln+Gln/Gln versus Arg/Arg: OR=1.35, 95% CI=0.89–2.05; Gln/Gln versus Arg/Gln+Arg/Arg: OR=1.37, 95% CI=0.93–2.02). This meta-analysis supported that IL-13 SNP rs20541 was associated with AR, particularly in Asians.