Duced the recruitment of monocytes to the infected peritoneum (Figure 1DDuced the recruitment of monocytes

Duced the recruitment of monocytes to the infected peritoneum (Figure 1D
Duced the recruitment of monocytes to the infected peritoneum (Figure 1D, 6-OHDA vs. SPLX + 6-OHDA). Conclusion: These results suggest that splenic nerve-derived catecholamines regulate the egress of splenic monocytes during infection and that altering this pathway can alter survival during septic peritonitis in mice. These data highlight the emerging role of splenic monocytes during inflammation and infection [1] and add to the body of evidence that the immunosuppressive effects of catecholamines can impair innate immune responses during infection [2]. These experiments may have important implications for patients receiving vasopressors in the ICU. References 1. Swirski FK, Nahrendorf M, Etzrodt M, et al: Identification of splenic reservoir monocytes and their deployment to inflammatory sites. Science 2009, 325:612-616. 2. Wong CH, Jenne CN, Lee WY, Leger C, Kubes P: Functional innervation of hepatic iNKT cells is immunosuppressive following stroke. Science 2011, 334:101-105. P72 Mannose-binding lectin deficiency and NOD2 mutations do not predispose to Staphylococcus aureus bloodstream infections but may influence outcome M Osthoff1*, HM Au Yong1, MM Dean2, D Eisen1 1 Royal Melbourne Hospital, Victorian Infectious Diseases Service, Parkville, Australia; 2Australian Red Cross Blood Service, Brisbane, Australia Critical Care 2012, 16(Suppl 3):P72 Background: Staphylococcus aureus is a major cause of bloodstream infections (BSI), and is associated with a higher morbidity and mortality compared with other BSI pathogens. Innate pattern recognition receptors like mannose-binding lectin (MBL) of the get Quisinostat complement system and NOD2 (nucleotide-binding oligomerization domain-containing protein 2), an intracellular sensor for a variety of pathogens, have been shown to be crucially involved in the immune response against S. aureus in knockout animal models [1,2], but human data are lacking. Low MBL levels and NOD2 mutations can be PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28607003 found in up to 30 and 10 in the general population, respectively [3,4]. This study aimed to investigate whether MBL deficiency and NOD2 mutations predispose to and influence the severity of S. aureus BSI. Methods: A matched case-control study was undertaken involving 70 patients with S. aureus BSI and 70 age-matched and sex-matched hospitalized controls recruited prospectively at two major tertiary hospitals. Participant blood samples were analyzed for MBL levels by mannan-binding ELISA and for four MBL2 and three NOD2 polymorphisms by real-time PCR. Clinical and microbiological data were reviewed. MBL deficiency was defined as functional MBL level 0.1 g/ml. Univariate and multivariate conditional logistic regression was used to investigate the risk of BSI in matched controls and cases. Results: S. aureus BSI were nosocomially acquired (60 ) and intravenous catheter associated (50 ) in the majority of cases with an in-hospital mortality of 10 . After adjusting for diabetes, immunosuppression, chronic kidney disease and long-term intravenous catheters, MBL deficiency was found less frequently in cases than controls (8.6 vs. 20 , OR = 0.38, P = 0.07) as were low-producing MBL genotypes (11 vs. 23 , OR = 0.37, P = 0.05), whereas NOD2 polymorphisms were similarly distributed (14 vs. 10 , P = 0.4). In line with MBL2 genotypic results, MBL levels were significantly higher in cases than in controls (adjusted OR = 1.35 per 1 g/ml increase, P = 0.002; Figure 1). Cases with NOD2 polymorphisms had less severe disease manifestation.