gynecology and obstetrics medical project, gynecology journal, obstetrics, gynecologic oncology, reproductive medicine, gynecological endoscopy, ultrasonography, gynecology articles

Ginekologia i Poloznictwo
ISSN 1896-3315 e-ISSN 1898-0759

The role of chosen polymorphism of gens coding cytokinesIL-1?, IL1ra, IL-6 and TNF? in the pathogenesisof the preterm delivery



Inflammation is a known risk factor for preterm delivery (PTD). Infection in pregnant womanis responsible for up to 40% cases of PTD. Intrauterine invasion of germs, chorioamonitis,sepsis, urinary tract infections, malaria, pneumonia are diseases with proven connection withPTD. Hyper- or hypostimulation of immune system in pregnant woman may lead to inappro-priate reaction for stimuli (e.g. infection), resulting in ripening of cervix, preterm prematurerupture of membranes (PPROM), uterus contractility and PTD. Interleukines are proteins, which are produced as a response for inflammation. They regulateall processes that help fight infection and provide healing. As other proteins the productionof interleukines is regulated by DNA. Changes in DNA like polymorphisms are responsiblefor e.g. inadequate production of interleukines or production of inactive praticles of protein.Single nucleotide polymorphism (SNP) is a change in one particular place in DNA chain (calledlocus) that is defined as a replacement in one of nucleic alkali to another.The interleukine-1 beta (IL-1ß), interleukine-6 (IL-6) and tumor necrosis factor alfa (TNFα)are proinflammatory cytokines. Particular polimorphisms in genes that codes these proteins(i.e. IL1B+3953, IL6-174 and TNFA-308 respectively) induce the inadequate production ofcytokines resulting in PPROM and PTD.Interleukine-1 receptor antagonist (IL1ra) is antyinflammatory cytokine that bounds compe-titively with receptor for IL-1ß but gives any biological effect typical for proinflammatory IL-1b. Polymorphism in intron 2 of interleukine-1 receptor antagonist gene (IL1RN) reducesproduction of IL1ra, which affects balance between IL1ra and IL-1ß and leads to inadequateinflammatory response and PTD.

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