scholarly journals Perinatal Gene-Gene and Gene-Environment Interactions on IgE Production and Asthma Development

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Jen-Chieh Chang ◽  
Lin Wang ◽  
Rong-Fu Chen ◽  
Chieh-An Liu

Atopic asthma is a complex disease associated with IgE-mediated immune reactions. Numerous genome-wide studies identified more than 100 genes in 22 chromosomes associated with atopic asthma, and different genetic backgrounds in different environments could modulate susceptibility to atopic asthma. Current knowledge emphasizes the effect of tobacco smoke on the development of childhood asthma. This suggests that asthma, although heritable, is significantly affected by gene-gene and gene-environment interactions. Evidence has recently shown that molecular mechanism of a complex disease may be limited to not only DNA sequence differences, but also gene-environmental interactions for epigenetic difference. This paper reviews and summarizes how gene-gene and gene-environment interactions affect IgE production and the development of atopic asthma in prenatal and childhood stages. Based on the mechanisms responsible for perinatal gene-environment interactions on IgE production and development of asthma, we formulate several potential strategies to prevent the development of asthma in the perinatal stage.

2020 ◽  
Vol 9 (8) ◽  
pp. 2633 ◽  
Author(s):  
Alain Calender ◽  
Thomas Weichhart ◽  
Dominique Valeyre ◽  
Yves Pacheco

Sarcoidosis is a complex disease that belongs to the vast group of autoinflammatory disorders, but the etiological mechanisms of which are not known. At the crosstalk of environmental, infectious, and genetic factors, sarcoidosis is a multifactorial disease that requires a multidisciplinary approach for which genetic research, in particular, next generation sequencing (NGS) tools, has made it possible to identify new pathways and propose mechanistic hypotheses. Codified treatments for the disease cannot always respond to the most progressive forms and the identification of new genetic and metabolic tracks is a challenge for the future management of the most severe patients. Here, we review the current knowledge regarding the genes identified by both genome wide association studies (GWAS) and whole exome sequencing (WES), as well the connection of these pathways with the current research on sarcoidosis immune-related disorders.


2020 ◽  
Vol 13 ◽  
Author(s):  
Theodora Katsila ◽  
Dimitrios Kardamakis

Background: Malignant gliomas constitute a complex disease phenotype that demands optimum decisionmaking. Despite being the most common type of primary brain tumors, gliomas are highly heterogeneous when their pathophysiology and response to treatment are considered. Such inter-individual variability also renders differential and early diagnosis extremely difficult. Recent evidence highlight that the gene-environment interplay becomes of fundamental importance in oncogenesis and progression of gliomas. Objective: To unmask key features of the gliomas disease phenotype and map the inter-individual variability of patients, we explore genotype-to-phenotype associations. Emphasis is put on microRNAs as they regulate gene expression, have been implicated in the pathogenesis of gliomas and may serve as theranostics, empowering non-invasive strategies (circulating free or in exosomes). Method: We mined text and omic datasets (as of 2019) and conducted a mixed-method content analysis. A novel framework was developed to meet the aims of our analysis, interrogating data in terms of content and context. We relied on literature data from PubMed/Medline and Scopus, as they are considered the largest abstract and citation databases of peer-reviewed literature. To avoid selection biases, both publicly available and private texts have been assessed. Both percent agreement and Cohen's kappa statistic have been calculated to avoid biases by SAS macro MAGREE with multicategorical ratings. Results: Gliomas serve as a paradigm for multifaceted datasets, despite data sparsity and scarcity. miRNAs and miRNAbased therapeutics are ready for prime time. Exosomal miRNAs empower non-invasive strategies, surpassing circulating free miRNAs, when accuracy and precision are considered. Conclusion: miRNAs holds promise as theranostics.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yu Zhang ◽  
Li Hua ◽  
Quan-Hua Liu ◽  
Shu-Yuan Chu ◽  
Yue-Xin Gan ◽  
...  

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.


BioTech ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 3
Author(s):  
Yinhao Du ◽  
Kun Fan ◽  
Xi Lu ◽  
Cen Wu

Gene-environment (G×E) interaction is critical for understanding the genetic basis of complex disease beyond genetic and environment main effects. In addition to existing tools for interaction studies, penalized variable selection emerges as a promising alternative for dissecting G×E interactions. Despite the success, variable selection is limited in terms of accounting for multidimensional measurements. Published variable selection methods cannot accommodate structured sparsity in the framework of integrating multiomics data for disease outcomes. In this paper, we have developed a novel variable selection method in order to integrate multi-omics measurements in G×E interaction studies. Extensive studies have already revealed that analyzing omics data across multi-platforms is not only sensible biologically, but also resulting in improved identification and prediction performance. Our integrative model can efficiently pinpoint important regulators of gene expressions through sparse dimensionality reduction, and link the disease outcomes to multiple effects in the integrative G×E studies through accommodating a sparse bi-level structure. The simulation studies show the integrative model leads to better identification of G×E interactions and regulators than alternative methods. In two G×E lung cancer studies with high dimensional multi-omics data, the integrative model leads to an improved prediction and findings with important biological implications.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Josefin Werme ◽  
Sophie van der Sluis ◽  
Danielle Posthuma ◽  
Christiaan A. de Leeuw

A Correction to this paper has been published: https://doi.org/10.1038/s41398-021-01334-6


2010 ◽  
Vol 10 (1) ◽  
Author(s):  
Stephen W Turner ◽  
Jon G Ayres ◽  
Tatiana V Macfarlane ◽  
Anil Mehta ◽  
Gita Mehta ◽  
...  

Genes ◽  
2021 ◽  
Vol 12 (8) ◽  
pp. 1181
Author(s):  
Alessandro Maglione ◽  
Miriam Zuccalà ◽  
Martina Tosi ◽  
Marinella Clerico ◽  
Simona Rolla

As a complex disease, Multiple Sclerosis (MS)’s etiology is determined by both genetic and environmental factors. In the last decade, the gut microbiome has emerged as an important environmental factor, but its interaction with host genetics is still unknown. In this review, we focus on these dual aspects of MS pathogenesis: we describe the current knowledge on genetic factors related to MS, based on genome-wide association studies, and then illustrate the interactions between the immune system, gut microbiome and central nervous system in MS, summarizing the evidence available from Experimental Autoimmune Encephalomyelitis mouse models and studies in patients. Finally, as the understanding of influence of host genetics on the gut microbiome composition in MS is in its infancy, we explore this issue based on the evidence currently available from other autoimmune diseases that share with MS the interplay of genetic with environmental factors (Inflammatory Bowel Disease, Rheumatoid Arthritis and Systemic Lupus Erythematosus), and discuss avenues for future research.


2010 ◽  
Vol 125 (2) ◽  
pp. 321-327.e13 ◽  
Author(s):  
Hao Wu ◽  
Isabelle Romieu ◽  
Min Shi ◽  
Dana B. Hancock ◽  
Huiling Li ◽  
...  

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