Household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case–control study

Abstract Background A number of studies have examined the association between mold exposure and childhood asthma. However, the conclusions were inconsistent, which might be partly attributable to the lack of consideration of gene function, especially the key genes affecting the pathogenesis of childhood asthma. Research on the interactions between genes and mold exposure on childhood asthma is still very limited. We therefore examined whether there is an interaction between inflammation-related genes and mold exposure on childhood asthma. Methods A case–control study with 645 asthmatic children and 910 non-asthmatic children aged 3–12 years old was conducted. Eight single nucleotide polymorphisms (SNPs) in inflammation-related genes were genotyped using MassARRAY assay. Mold exposure was defined as self-reported visible mold on the walls. Associations between visible mold exposure, SNPs and childhood asthma were evaluated using logistic regression models. In addition, crossover analyses were used to estimate the gene-environment interactions on childhood asthma on an additive scale. Results After excluding children without information on visible mold exposure or SNPs, 608 asthmatic and 839 non-asthmatic children were included in the analyses. Visible mold exposure was reported in 151 asthmatic (24.8%) and 119 non-asthmatic children (14.2%) (aOR 2.19, 95% CI 1.62–2.97). The rs7216389 SNP in gasdermin B gene (GSDMB) increased the risk of childhood asthma with each C to T substitution in a dose-dependent pattern (additive model, aOR 1.32, 95% CI 1.11–1.57). Children carrying the rs7216389 T allele and exposed to visible mold dramatically increased the risk of childhood asthma (aOR 3.21; 95% CI 1.77–5.99). The attributable proportion due to the interaction (AP: 0.47, 95% CI 0.03–0.90) and the relative excess risk due to the interaction (RERI: 1.49, 95% CI 0–2.99) were statistically significant. Conclusions In the present study, there was a significant additive interaction between visible mold exposure and rs7216389 SNP on childhood asthma. Future studies need to consider the gene-environment interactions when exploring the risk factors of childhood asthma.

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Association Between Tfeb Gene Polymorphism, Gene–environment Interaction, and Fatty Liver Disease: a Case–control Study in China

10.21203/rs.3.rs-541251/v1 ◽

2021 ◽

Author(s):

Chunbao Mo ◽

Tingyu Mai ◽

Jiansheng Cai ◽

Haoyu He ◽

Huaxiang Lu ◽

...

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Fatty Liver Disease ◽

Case Control Study ◽

Case Control ◽

Environment Interaction ◽

Additive Interaction ◽

Gene Environment Interaction ◽

Gene Environment ◽

Control Study

Abstract Background: Fatty liver disease (FLD) is a serious public health problem that is rapidly increasing. Evidences indicated that the transcription factor EB (TFEB) gene may be involved in the pathophysiology of FLD; however, whether TEFB polymorphism is association with FLD remains unclear.Objectives: To explore the association among TFEB polymorphism, gene–environment interaction, and FLD and provide epidemiological evidence for clarifying the genetic factors of FLD.Methods: This study is a case–control study. Sequenom MassARRAY was applied in genotyping. Logical regression was used to analyze the association between TFEB polymorphism and FLD, and the gene–environment interaction in FLD was evaluated by multiplication and additive interaction models.Results: (1) The alleles and genotypes of each single nucleotide polymorphism of TFEB in the case and control groups were evenly distributed; no statistically substantial difference was observed. (2) Logistic regression analysis indicated that TFEB polymorphism is not remarkably associated with FLD. (3) In the multiplicative interaction model, rs1015149, rs1062966, and rs11754668 had remarkable interaction with smoking amount. Rs1062966 and rs11754668 also had a considerable interaction with body mass index and alcohol intake, respectively. However, no remarkable additive interaction was observed.Conclusion: TFEB polymorphism is not directly associated with FLD susceptibility, but the risk can be changed through gene–environment interaction.

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A CASE CONTROL STUDY ON DETERMINANTS OF CHILDHOOD ASTHMA IN SCHOOL CHIL-DREN OF CHITRADURGA CITY

International Journal of Current Pharmaceutical Research ◽

10.22159/ijcpr.2018v10i3.27335 ◽

2018 ◽

Vol 10 (3) ◽

pp. 39

Author(s):

Prakruthi G. M. ◽

Bharathi D. R. ◽

Yogananda R.

Keyword(s):

Childhood Asthma ◽

Case Control Study ◽

Case Control ◽

Age Group ◽

Community Based ◽

Chi Square ◽

Asthmatic Children ◽

Chi Square Test ◽

Strength Of Association ◽

Control Study

Objective: Asthma is a chronic airway inflammatory disease in which many cells and cellular elements play a role often arising from allergies, subsequently cause shortness of breath, wheezing and coughing it affects children in different ways. To study the sociodemographic characteristics of asthmatic children and compare the predisposing factors of asthma in children.Methods: A Community based Case control study in selected schools in chitradurga for a period of 6 mo. A total of 90 children, among which 30 asthma children and 60 non asthma children were participated. Odds ratio will be calculated to know the strength of association. chi square test will be calculated to the significance.Results: A total of 90 children aged<14 y data. Female children are more exposed to asthma than male. In childhood asthma age group between 10-14years the age group of 10 y(26.7%) and 12 y (26.7%) were more exposed to the asthma.Conclusion: In Chitradurga city, the study area, is of no exception with regard to case control. From the total of 90 children selected for the study majority were found risk factors affected. It was due to their family history, exposure to pet animals, allergy, age group, BMI and sex.

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Association between TFEB gene polymorphism, gene–environment interaction, and fatty liver disease: A case–control study in China

Science Progress ◽

10.1177/00368504211043766 ◽

2021 ◽

Vol 104 (3) ◽

pp. 003685042110437

Author(s):

Chunbao Mo ◽

Tingyu Mai ◽

Jiansheng Cai ◽

Haoyu He ◽

Huaxiang Lu ◽

...

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Fatty Liver Disease ◽

Case Control Study ◽

Case Control ◽

Environment Interaction ◽

Additive Interaction ◽

Gene Environment Interaction ◽

Gene Environment ◽

Control Study

Background: Fatty liver disease (FLD) is a serious public health problem that is rapidly increasing. Evidence indicates that the transcription factor EB ( TFEB) gene may be involved in the pathophysiology of FLD; however, whether TEFB polymorphism has an association with FLD remains unclear. Objectives: To explore the association among TFEB polymorphism, gene–environment interaction, and FLD and provide epidemiological evidence for clarifying the genetic factors of FLD. Methods: This study is a case–control study. Sequenom MassARRAY was applied in genotyping. Logical regression was used to analyze the association between TFEB polymorphism and FLD, and the gene–environment interaction in FLD was evaluated by multiplication and additive interaction models. Results: (1) The alleles and genotypes of each single nucleotide polymorphism and haplotypes of TFEB in the case and control groups were evenly distributed; no statistically substantial difference was observed. (2) Logistic regression analysis indicated that TFEB polymorphism is not remarkably associated with FLD. (3) In the multiplicative interaction model, rs1015149, rs1062966, rs11754668 and rs2273068 had remarkable interaction with the amount of cigarette smoking. Rs1062966 and rs11754668 also had a considerable interaction body mass index and alcohol intake, respectively. However, no remarkable additive interaction was observed. Conclusion: TFEB polymorphism is not directly associated with FLD susceptibility, but the risk can be changed through gene–environment interaction.

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The association between seropositivity to human toxocariasis and childhood asthma in northern Iran: a case-control study

Allergologia et Immunopathologia ◽

10.15586/aei.v49i1.15 ◽

2021 ◽

Vol 49 (1) ◽

pp. 25-31

Author(s):

Sorena Darvish ◽

Iraj Mohammadzadeh ◽

Saeed Mehravar ◽

Adel Spotin ◽

Ali Rostami

Keyword(s):

Childhood Asthma ◽

Case Control Study ◽

Immunoglobulin E ◽

Case Control ◽

Enzyme Linked Immunosorbent Assay ◽

P Value ◽

Case Group ◽

Northern Iran ◽

Asthmatic Children ◽

Control Study

Background: Besides the well-known risk factors, Toxocara infection is thought to play a significant etiological role in the development of childhood asthma. To further explore this association, the prevalence of Toxocara infection in sera of asthmatic children and healthy controls in northern Iran was investigated. Methods: In this case-control study, cases were 145 physician-confirmed asthmatic children diagnosed according to the Global Initiative for Asthma (GINA) guidelines. Controls were 115 age–sex–residence-matched children who did not have physician-diagnosed asthma. The presence of anti-Toxocara immunoglobulin G (IgG) was tested using enzyme-linked immunosorbent assay. Univariate and multivariate logistic regression methods were used for case-control comparisons. Results: Seropositivity rate was 4.1% (95% CI, 3.4–4.7%) in asthmatic children and 0.86% (95% CI, 0.71–1.0%) in controls, suggesting a strong association (P-value < 0.02). Moreover, Toxocara infection was not significantly more prevalent (P-value = 0.12) in children with moderate sustainable asthma (9.3%, 3/32) than in children with mild sustainable asthma (2.3%, 3/113). Mean total immunoglobulin E (IgE) level was significantly higher in Toxocara-infected children (222.3 ± 367.1) than in non-infected children (143.19 ± 218.05) in the case group (P-value < 0.05). Conclusions: Our findings indicated that Toxocara infection can play an important role in childhood asthma. Further experimental and epidemiological studies are needed to clarify this hypothesis.

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Correction to: Associations between prenatal exposure to cadmium and lead with neural tube defect risks are modified by single-nucleotide polymorphisms of fetal MTHFR and SOD2: a case–control study

Environmental Health ◽

10.1186/s12940-021-00762-7 ◽

2021 ◽

Vol 20 (1) ◽

Author(s):

Mengyuan Liu ◽

Jinhui Yu ◽

Zaiming Su ◽

Ying Sun ◽

Yaqiong Liu ◽

...

Keyword(s):

Single Nucleotide Polymorphisms ◽

Prenatal Exposure ◽

Neural Tube ◽

Neural Tube Defect ◽

Case Control Study ◽

Case Control ◽

Nucleotide Polymorphisms ◽

Single Nucleotide ◽

Cadmium And Lead ◽

Control Study

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Single nucleotide polymorphisms of TRAF2 and TRAF5 gene in ankylosing spondylitis: a case–control study

Clinical and Experimental Medicine ◽

10.1007/s10238-021-00719-7 ◽

2021 ◽

Author(s):

Shanshan Xu ◽

Jiangping Kong ◽

Li Huang ◽

Huimin Xie ◽

Feier Wang ◽

...

Keyword(s):

Ankylosing Spondylitis ◽

Single Nucleotide Polymorphisms ◽

Case Control Study ◽

Case Control ◽

Nucleotide Polymorphisms ◽

Single Nucleotide ◽

Control Study

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An ADAM33 Polymorphism Associates with Progression of Preschool Wheeze into Childhood Asthma: A Prospective Case-Control Study with Replication in a Birth Cohort Study

PLoS ONE ◽

10.1371/journal.pone.0119349 ◽

2015 ◽

Vol 10 (3) ◽

pp. e0119349 ◽

Cited By ~ 10

Author(s):

Ester M. M. Klaassen ◽

John Penders ◽

Quirijn Jöbsis ◽

Kim D. G. van de Kant ◽

Carel Thijs ◽

...

Keyword(s):

Cohort Study ◽

Birth Cohort ◽

Childhood Asthma ◽

Case Control Study ◽

Case Control ◽

Birth Cohort Study ◽

Control Study ◽

Prospective Case Control Study

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Association between CTSS gene polymorphism and the risk of acute atherosclerotic cerebral infarction in Chinese population: a case–control study

Bioscience Reports ◽

10.1042/bsr20180586 ◽

2018 ◽

Vol 38 (6) ◽

Cited By ~ 2

Author(s):

Lian Luo ◽

Mingli Zhu ◽

Jiajun Zhou

Keyword(s):

Cerebral Infarction ◽

Case Control Study ◽

Case Control ◽

Cathepsin S ◽

Control Group ◽

Study Group ◽

Nucleotide Polymorphisms ◽

Single Nucleotide ◽

Independent Risk Factors ◽

Control Study

Objective: To investigate the association between the gene polymorphisms of rs774320676, rs768437857, rs928508030, and rs2275235 loci of Cathepsin S (CTSS) and risk of acute atherosclerotic cerebral infarction. Methods: A total of 315 patients with acute atherosclerotic cerebral infarction (study group) and 220 healthy subjects (control group) were enrolled in the present study. The genetic polymorphism of rs774320676, rs768437857, rs928508030, and rs2275235 loci of CTSS of subjects was analyzed by PCR-Sanger sequencing. Results: The proportion of carriers with mutant T allele at rs774320676 locus and mutant G allele at rs928508030 locus of CTSS in study group was significantly higher than the proportion in control group (P=0.000, adjusted odds ratio (OR) = 1.332, 95% confidence interval (CI) = 1.200–1.460; P<0.001, adjusted OR = 1.185, 95% CI = 1.055–1.314; P=0.002). The T allele at rs774320676 locus and the G allele at rs928508030 locus of CTSS were independent risk factors for acute atherosclerotic cerebral infarction (OR = 2.534, 95% CI = 1.020–4.652, P=0.006; OR = 2.016, 95% CI = 1.031–4.385, P=0.031). Conclusion: The single nucleotide polymorphisms (SNPs) of rs774320676 and rs928508030 of CTSS gene were related with risk for acute atherosclerotic cerebral infarction. The T allele at rs774320676 locus and G allele at rs928508030 locus of CTSS were genetic susceptibility genes of acute atherosclerotic cerebral infarction.

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