%0 Generic %A N.J., Shubin %A T.N., Pham %A K.L., Staudenmayer %A B.A., Parent %A Q., Qiu %A G.E., O’Keefe %D 2018 %T Supplementary Material for: A Potential Mechanism for Immune Suppression by Beta-Adrenergic Receptor Stimulation following Traumatic Injury %U https://karger.figshare.com/articles/dataset/Supplementary_Material_for_A_Potential_Mechanism_for_Immune_Suppression_by_Beta-Adrenergic_Receptor_Stimulation_following_Traumatic_Injury/5896498 %R 10.6084/m9.figshare.5896498.v1 %2 https://karger.figshare.com/ndownloader/files/10502947 %2 https://karger.figshare.com/ndownloader/files/10502950 %2 https://karger.figshare.com/ndownloader/files/10502953 %2 https://karger.figshare.com/ndownloader/files/10502956 %K Host defense %K Immune response %K Kinase %K Phosphatase %K Protein %K Sepsis %X Background: β-Adrenergic agents suppress inflammation and may play an important role in posttraumatic infections. Mechanisms may include inhibition of MAP kinase signaling. We sought to determine whether MKP-1 contributed to catecholamine suppression of innate immunity and also wanted to know whether early catecholamine treatment after traumatic injury increases the risk of later nosocomial infection. Methods: We performed experiments using THP-1 cells and peripheral blood mononuclear cells from healthy individuals. We exposed cells to epinephrine and/or LPS and measured inflammatory gene transcription and MAP kinase activation. We inhibited MKP-1 activity to determine its role in catecholamine-induced immune suppression. Finally, we studied injured subjects to determine whether early catecholamine treatment was associated with nosocomial infection. Results: Epinephrine increases MKP-1 transcripts and protein and decreases LPS-induced p38 and JNK phosphorylation and TNF-α gene transcription. RNAi inhibition of MKP-1 at least partially restores LPS-induced TNF-α gene expression (p = 0.024). In the clinical cohort, subjects treated with β-adrenergic agents had an increased risk of ventilator-associated pneumonia (aOR = 1.9; 95% CI = 1.3–2.6) and bacteremia (aOR = 1.5; 95% CI = 1.1–2.3). Conclusions: MKP-1 may have a role in catecholamine-induced suppression of innate immunity, and exogenous catecholamines might contribute to nosocomial infection risk. %I Karger Publishers