Background: IL12A has been implicated in T-cell development and may thus influence the development of atopy and allergic diseases.
Methods: We tested for association between four linkage disequilibrium (LD)-tagging SNPs (rs2243123, rs2243151, rs668998, and rs17826053) in IL12A and asthma and allergy-related (serum total and allergen-specific IgE, and skin test reactivity [STR] to two common allergens) phenotypes in two samples: 417 Costa Rican children with asthma and their parents, and 470 families of 503 white children in the Childhood Asthma Management Program (CAMP). The analysis was conducted using the family-based association test (FBAT) statistic implemented in the PBAT program.
Results: Among Costa Rican children with asthma, homozygosity for the minor allele of each of two SNPs in IL12A (rs2243123 and rs2243151) was associated with increased risks of STR to American cockroach (P = 0.03 for both SNPs), STR to German cockroach (P = 0.01 for both SNPs), and having a positive IgE to German cockroach (P < 0.05 for both SNPs). Among children in CAMP, homozygosity for the minor allele of SNP rs2243151 in IL12A was inversely associated with STR to German cockroach (P = 0.03) and homozygosity for the minor allele of SNP rs17826053 in IL12A was associated with increased risks of STR to American cockroach (P = 0.01) and STR to German cockroach (P = 0.007). There was no significant association between any SNP in IL12A and asthma, STR to dust mite, or total IgE in Costa Rica or CAMP.
Conclusion: Our findings suggest that variants in IL12A influence cockroach allergy among children with asthma.
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http://dx.doi.org/10.1186/1476-7961-6-6 | DOI Listing |
JAMA Pediatr
January 2025
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Importance: Spontaneous reports have indicated that montelukast increases the risk of neuropsychiatric adverse events, and the US Food and Drug Administration added a boxed warning about these risks in 2020. However, the potential mechanism is not well understood, and the observational evidence is scarce, particularly in children.
Objective: To assess the potential association between the use of montelukast and the risk of neuropsychiatric adverse events in children and adolescents.
Am J Respir Crit Care Med
January 2025
Beth Israel Deaconess Medical Center, Pulmonary, Critical Care and Sleep Medicine, Boston, Massachusetts, United States.
Am J Respir Cell Mol Biol
January 2025
University of Groningen, University Medical Center Groningen, Department of Pulmonology and Pediatric Allergy, Beatrix Children's Hospital, Groningen, Netherlands.
Asthma is a genetically complex inflammatory airway disease associated with over 200 Single nucleotide polymorphisms (SNPs). However, the functional effects of many asthma-associated SNPs in lung and airway epithelial samples are unknown. Here, we aimed to conduct expression quantitative trait loci (eQTL) analysis using a meta-analysis of nasal and lung samples.
View Article and Find Full Text PDFJ Asthma
January 2025
Department of Pharmacology and Toxicology, University of Antioquia, Medellín, Colombia.
Introduction: Asthma imposes a critical economic burden on health systems, especially with the incorporation of new drugs. Recently, mepolizumab has been approved to prevent exacerbations in patients with eosinophilic asthma, however their high cost constitutes a barrier for their use, especially in middle- and low-income countries. This study aimed to estimate the economically justifiable price of mepolizumab for preventing exacerbations in patients with severe asthma in Colombia.
View Article and Find Full Text PDFAm J Physiol Lung Cell Mol Physiol
January 2025
Division of Pulmonology, Asthma, Cystic Fibrosis, and Sleep, Emory University School of Medicine, Atlanta, GA, USA.
Secondhand smoke exposure (SHSe) is a public health threat for people with cystic fibrosis (CF) and other lung diseases. Primary smoking reduces CFTR channel function, the causative defect in CF. We reported that SHSe worsens respiratory and nutritional outcomes in CF by disrupting immune responses and metabolic signaling.
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