Inflammation is a known risk factor for preterm delivery (PTD). Infection in pregnant woman is responsible for up to 40% cases of PTD. Intrauterine invasion of germs, chorioamonitis, sepsis, urinary tract infections, malaria, pneumonia are diseases with proven connection with PTD. Hyper- or hypostimulation of immune system in pregnant woman may lead to inappropriate reaction for stimuli (e.g. infection), resulting in ripening of cervix, preterm premature rupture of membranes (PPROM), uterus contractility and PTD. Interleukines are proteins, which are produced as a response for inflammation. They regulate all processes that help fight infection and provide healing. As other proteins the production of interleukines is regulated by DNA. Changes in DNA like polymorphisms are responsible for 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 (called locus) 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 of cytokines resulting in PPROM and PTD. Interleukine-1 receptor antagonist (IL1ra) is antyinflammatory cytokine that bounds competitively 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) reduces production of IL1ra, which affects balance between IL1ra and IL-1ß and leads to inadequate inflammatory response and PTD.