“…32 There is evidence that variants of the NOD2 gene, 33,34 and various TLR 35 there was increased transition of pathological BT to culture-positive SBP in the case of the same NOD2 variant. 37,38 Furthermore, TLR2 (−16934 T>A, rs4696480) and TLR4 (D299G, rs4986790) polymorphisms were associated with an increased systemic antigen burden as well, described by the serum level of lipoteichoic acid, LPS, and bacterial-DNA. 35 In our study we applied both serological and clinical approaches to assess the impact of PRR genetic variants to BT.…”