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Preterm birth and genitourinary tract infections: assessing gene-environment interaction
Dario Elias1,2, Lucas Gimenez1,2,3, Fernando Poletta1,2,3
1Laboratorio de Epidemiología Genética Centro de Educación Médica e Investigaciones Clínicas-Consejo Nacional de Investigaciones Científicas y Técnicas (CEMIC-CONICET), Centro de Educación Médica e Investigaciones Clínicas-Consejo Nacional de Investigaciones Científicas y Técnicas (CEMIC-CONICET), Ciudad Autónoma de Buenos Aires, Argentina.
Insights
Genetic and infection interactions increase preterm birth risk. Specific gene variants and infections, like vaginal-urinary tract infections (VI-UTI), heighten prematurity risk depending on clinical subtype and maternal/fetal genotypes.
Area of Science:
- Genetics
- Obstetrics
- Infectious Diseases
Background:
- Preterm birth (PTB) is a leading global cause of perinatal mortality.
- The etiology of PTB is complex, involving genetic and environmental factors.
- Understanding gene-environment interactions is crucial for PTB prevention.
Purpose of the Study:
- To investigate the statistical interaction between genes and vaginal-urinary tract infections (VI-UTI) in relation to PTB risk.
- To analyze these interactions across different clinical subtypes of PTB.
- To identify specific genetic variants and infection types contributing to PTB risk.
Main Methods:
- Genotyping of 24 single nucleotide polymorphisms (SNPs) in 18 candidate genes.
- Analysis of 352 fetal triads and 106 maternal triads.
- Conditional logistic regression and genotypic transmission/disequilibrium tests to evaluate statistical interactions.
Main Results:
- Specific fetal SNPs (e.g., rs11686474, rs4458044, rs883319, rs2277698, rs5742612) and maternal SNPs (e.g., rs1882435, rs4458044) were associated with increased PTB risk.
- Interactions varied by infection type (UTI vs. VI), maternal/fetal genotype, and PTB clinical subtype (idiopathic, PPROM, spontaneous).
- Notable associations were found in PTB-idiopathic, PPROM, and spontaneous PTB subtypes.
Conclusions:
- Maternal and fetal genes involved in inflammatory/infectious and hormonal regulation processes interact with VI-UTI to increase PTB risk.
- These gene-infection interactions are specific to PTB clinical subtypes and infection types.
- Findings contribute to understanding PTB etiology and may inform prevention strategies.
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.
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