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Functional polymorphisms of various PRR<\/jats:styled-content>s have been established to contribute to an increased susceptibility to spontaneous bacterial peritonitis (SBP<\/jats:styled-content>). Their role in the development of cirrhosis\u2010associated bacterial infections (BI<\/jats:styled-content>), beyond SBP<\/jats:styled-content> or progressive disease course related to pathological bacterial translocation (BT<\/jats:styled-content>) remains unknown.<\/jats:p><\/jats:sec>Methods<\/jats:title>Three hundred and forty\u2010nine patients with cirrhosis were genotyped for common NOD<\/jats:styled-content>2<\/jats:italic> (R702W, G908R and L1007PfsinsC), TLR<\/jats:styled-content>2<\/jats:italic> (\u221216934T>A), and TLR<\/jats:styled-content>4<\/jats:italic> (D299G) variants. Incidence of BI<\/jats:styled-content>s, decompensating events and liver\u2010related death were assessed in a 5\u2010year follow\u2010up observational study. Pathological BT<\/jats:styled-content> was assessed based on the presence of antimicrobial antibodies or lipopolysaccharide\u2010binding protein (LBP<\/jats:styled-content>) level.<\/jats:p><\/jats:sec>Results<\/jats:title>In patients with ascites (n\u00a0=\u00a088) only NOD<\/jats:styled-content>2<\/jats:italic> gene variants were associated with an increased cumulative probability of SBP<\/jats:styled-content> (76.9%\u00a0\u00b1\u00a019.9%) compared to wild\u2010type (30.9%\u00a0\u00b1\u00a06.9%, P<\/jats:italic>LogRank<\/jats:sub>\u00a0=\u00a0.047). Individual or combined PRR<\/jats:styled-content> genetic profiles were associated with the risk of non\u2010SBP<\/jats:styled-content> type BI<\/jats:styled-content>. Advanced disease stage (HR<\/jats:styled-content> [95% CI<\/jats:styled-content>]: 2.11 [1.38\u20103.25]) and prior history of a BI<\/jats:styled-content> episode (HR<\/jats:styled-content>: 2.42 [1.58\u20103.72]) were the major clinical risk factors of a subsequent BI<\/jats:styled-content>. The risk of a non\u2010SBP<\/jats:styled-content> type BI<\/jats:styled-content> in patients with advanced disease and a prior BI<\/jats:styled-content> was even higher (HR<\/jats:styled-content>: 4.74 [2.68\u20108.39]). The frequency of antimicrobial antibodies and LBP<\/jats:styled-content> levels did not differ between various PRR<\/jats:styled-content> genotypes. Correspondingly, PRR<\/jats:styled-content> genetic profile was not able to predict the long\u2010term disease course.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>In cirrhosis, functional polymorphisms of PRR<\/jats:styled-content>s did not improve the identification of patients with high risk of BI<\/jats:styled-content> beyond SBP<\/jats:styled-content> or progressive diseases course.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.13664","type":"journal-article","created":{"date-parts":[[2017,12,13]],"date-time":"2017-12-13T06:45:32Z","timestamp":1513147532000},"page":"1242-1252","source":"Crossref","is-referenced-by-count":9,"title":["Functional polymorphisms of innate immunity receptors are not risk factors for the non\u2010SBP<\/scp> type bacterial infections in cirrhosis"],"prefix":"10.1111","volume":"38","author":[{"given":"Tamas","family":"Dinya","sequence":"first","affiliation":[{"name":"Faculty of Medicine Institute of Surgery University of Debrecen Debrecen 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