Preterm birth and genitourinary tract infections: assessing gene–environment interaction
| العنوان: | Preterm birth and genitourinary tract infections: assessing gene–environment interaction |
|---|---|
| المؤلفون: | Cesar Saleme, Jorge Santiago López Camelo, Hebe Campaña, Juan Antonio Gili, Rocio Uranga, Julia Ratowiecki, Viviana Cosentino, Fernando A. Poletta, Silvina L Heisecke, Dario Elias, Hugo Krupitzki, Lucas Gabriel Gimenez, Monica Rittler, Mariela Pawluk, María Rita Santos, Enrique C. Gadow |
| المصدر: | Pediatric Research. 90:678-683 |
| بيانات النشر: | Springer Science and Business Media LLC, 2020. |
| سنة النشر: | 2020 |
| مصطلحات موضوعية: | Fetus, Candidate gene, medicine.medical_specialty, business.industry, Obstetrics, Single-nucleotide polymorphism, medicine.disease, 03 medical and health sciences, 0302 clinical medicine, 030225 pediatrics, Pediatrics, Perinatology and Child Health, Etiology, Medicine, SNP, Gestation, Allele, business, Premature rupture of membranes, 030217 neurology & neurosurgery |
| الوصف: | Background Preterm birth (PTB) is the leading cause of perinatal morbimortality worldwide. Genetic and environmental factors could raise PTB risk. The aim of this study was to analyze the contribution of the statistical interaction between genes and vaginal-urinary tract infections (VI-UTI) to the risk of PTB by clinical subtype. Methods Twenty-four SNPs were genotyped in 18 candidate genes from 352 fetal triads and 106 maternal triads. Statistical interactions were evaluated with conditional logistic regression models based on genotypic transmission/disequilibrium test. Results In PTB-idiopathic subtype mothers exposed to UTI, fetal SNPs rs11686474 (FSHR), rs4458044 (CRHR1, allele G), rs883319 (KCNN3), and maternal SNP rs1882435 (COL4A3) showed a nominal significant increment in prematurity risk. In preterm premature rupture of membranes (PPROM), fetal SNP rs2277698 (TIMP2) showed a nominal significant risk increment. In mothers exposed to VI, fetal SNP rs5742612 (IGF1) in PTB-PPROM and maternal SNP rs4458044 (CRHR1, allele C) in spontaneous PTB showed nominal significant increment in prematurity risk. Conclusions Certain maternal and fetal genes linked to infectious/inflammatory and hormonal regulation processes increase prematurity risk according to clinical subtype when mothers are exposed to UTI or VI. These findings may help in the understanding of PTB etiology and PTB prevention. Impact Preterm birth is a major cause of perinatal morbimortality worldwide and its etiology remains unknown.This work provides evidence on the statistical interaction of six genes with gestational vaginal or urinary infections leading to the occurrence of preterm births. Statistical interactions vary according to infection type, genotype (maternal and fetal), and clinical subtype of prematurity.Certain maternal and fetal genetic variants of genes linked to infectious/inflammatory and hormonal regulation processes would increase the risk of prematurity according to clinical subtype and infection type.Our findings may help in the study of etiology of preterm birth and its prevention. |
| تدمد: | 1530-0447 0031-3998 |
| DOI: | 10.1038/s41390-020-01200-z |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_________::98a56cbb27806e774a8b3baa9d79aff2 https://doi.org/10.1038/s41390-020-01200-z |
| Rights: | CLOSED |
| رقم الانضمام: | edsair.doi...........98a56cbb27806e774a8b3baa9d79aff2 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15300447 00313998 |
|---|---|
| DOI: | 10.1038/s41390-020-01200-z |