Abstract
Clear inter-individual differences exist in the response to C. trachomatis (CT) infections and reproductive tract complications in women. Host genetic variation like single nucleotide polymorphisms (SNPs) have been associated with differences in response to CT infection, and SNPs might be used as a genetic component in a tubal-pathology predicting algorithm. Our aim was to confirm the role of four genes by investigating proven associated SNPs in the susceptibility and severity of a CT infection. A total of 1201 women from five cohorts were genotyped and analyzed for TLR2 + 2477 G > A, NOD1 + 32656 T −> GG, CXCR5 + 10950 T > C, and IL10 − 1082 A > G. Results confirmed that NOD1 + 32656 T −>GG was associated with an increased risk of a symptomatic CT infection (OR: 1.9, 95%CI: 1.1–3.4, p = 0.02), but we did not observe an association with late complications. IL10 − 1082 A > G appeared to increase the risk of late complications (i.e., ectopic pregnancy/tubal factor infertility) following a CT infection (OR = 2.8, 95%CI: 1.1–7.1, p = 0.02). Other associations were not found. Confirmatory studies are important, and large cohorts are warranted to further investigate SNPs’ role in the susceptibility and severity of a CT infection.
Highlights
C. trachomatis (CT) is the most diagnosed bacterial sexually transmittable infection (STI) worldwide [1], with an estimated 127 million new infections each year [2]
Disease pathology is based on the functionality of these four genes linked to the Single Nucleotide Polymorphisms (SNPs) studies
Women without CT antibodies but with a high genetic risk profile should be investigated in more detail instead of trying to become pregnant for a year longer
Summary
CT is the most diagnosed bacterial sexually transmittable infection (STI) worldwide [1], with an estimated 127 million new infections each year [2]. An estimated 70–80% of the infections are asymptomatic [4]. Estimating the individual risk of late complications is complicated by interpersonal differences in susceptibility, course, and outcome of the infection. These differences in women can at least to some extent be explained by bacterial factors (e.g., virulence, load), environmental factors (e.g., co-infection, microbiome), and host factors (e.g., immunogenetic differences between individuals, (sexual) risk behavior) [6,7]
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