165 Persistent MRSA bacteremia 8 Second, activation of STAT1 is known to induce T-helper cell polarization into the Th1, which tips the see-saw balance away from Th17-mediated interleukin-1 (IL1) and interleukin 17 (IL-17) production known to mediate neutrophil recruitment and activation critical for bactericidal activity. Third, in resolving persistent MRSAB patients, the hypomethylation in glucocorticoid receptor and associated co-factor p300 histone acetyltransferase promoter regions likely helps counter-regulate the life-threatening pro-inflammatory response that occurs during bloodstream infections [55]. Figure 2. Schematic showing genes with hypomethylation in patients with persistent MRSA bacteremia (PB) and resolving MRSA bacteremia (RB). Biomarkers for persistent SAB These studies represent a potential breakthrough in unraveling the astonishingly complex genomic and epigenetic distinctions between patients with persistent MRSAB and resolving MRSAB. The clearest application of this discovery is the potential to identify patients at risk for persistent MRSAB, which could lead to alterations of initial therapy, expediting of additional diagnostic evaluation, and the capacity to improve clinical outcomes. Concurrent work in identifying biomarkers in patients with persistent SAB and persistent MRSAB has identified a handful of possible candidates. Using a threshold of blood cultures positive for >5 days to define persistent SAB, Guimaraes et al. identified eight proteins correlating with persistent SAB, with interleukin 17A (IL-17A), IL-10, and soluble E-selectin levels, showing the most robust association [47]. A follow-up study by Cao et al. found levels of IL-17A, IL-10, or soluble E-selectin levels were able to individually identify patients at risk of
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