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Background  Pathways coordinated by innate pattern recognition receptors like mannose-binding lectin (MBL) and nucleotide-binding oligomerization domain 2 (NOD2) are among the first immune responses to   Staphylococcus aureus   (  S. aureus  ) bloodstream infections (BSI) in animal models, but human data are limited. Here, we investigated the role of MBL deficiency and  NOD2  mutations in the predisposition to and severity of   S. aureus   BSI.    Patients and Methods  A matched case-control study was undertaken involving 70 patients with   S. aureus   BSI and 70 age- and sex-matched hospitalized controls. MBL levels,  MBL2  and  NOD2  polymorphisms were analyzed.    Results  After adjusting for potential confounders, MBL deficiency (<0.5 µg/ml) was found less frequently in cases than controls (26 vs. 41%, OR 0.4, 95% confidence interval (CI) 0.20-0.95, p=0.04) as were low producing MBL genotypes (11 vs. 23%, OR 0.2, 95% CI 0.08-0.75, p=0.01), whereas  NOD2  polymorphisms were similarly distributed. Cases with  NOD2  polymorphisms had less organ dysfunction as shown by a lower SOFA score (median 2.5 vs. 4.5, p=0.02), whereas only severe MBL deficiency (<0.1 µg/ml) was associated with life-threatening   S. aureus   BSI (OR 5.6, 95% CI 1.25-24.85, p=0.02).    Conclusions  Contrary to animal model data, our study suggests MBL deficiency may confer protection against acquiring   S. aureus   BSI.  NOD2  mutations were less frequently associated with multi-organ dysfunction. Further human studies of the innate immune response in   S. aureus   BSI are needed to identify suitable host targets in sepsis treatment.

plos one

Significance of Mannose-Binding Lectin Deficiency and Nucleotide-Binding Oligomerization Domain 2 Polymorphisms in Staphylococcus aureus Bloodstream Infections: A Case-Control Study