Rapamycin Augments the NMDA-Mediated TNF Suppression of MRSA-Stimulated RAW264.7 Murine Macrophages

Background. Methicillin-resistant Staphylococcus aureus (MRSA) can stimulate massive cytokine release. Ketamine suppresses tumor necrosis factor (TNF) secretion by MRSA-stimulated RAW264.7 macrophages, and the mechanism likely involves N-methyl-D-aspartic acid (NMDA) receptor antagonism. The downstr...

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Main Authors: Thomas Spentzas, Rebekah K. H. Shappley, Fabio Savorgnan, Elizabeth Meals, B. Keith English
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:International Journal of Inflammation
Online Access:http://dx.doi.org/10.1155/2012/542727
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author Thomas Spentzas
Rebekah K. H. Shappley
Fabio Savorgnan
Elizabeth Meals
B. Keith English
author_facet Thomas Spentzas
Rebekah K. H. Shappley
Fabio Savorgnan
Elizabeth Meals
B. Keith English
author_sort Thomas Spentzas
collection DOAJ
description Background. Methicillin-resistant Staphylococcus aureus (MRSA) can stimulate massive cytokine release. Ketamine suppresses tumor necrosis factor (TNF) secretion by MRSA-stimulated RAW264.7 macrophages, and the mechanism likely involves N-methyl-D-aspartic acid (NMDA) receptor antagonism. The downstream effects of NMDA-mediated TNF suppression, specifically the PI3K/Akt and mTOR modulation, have not been described. Methods. RAW264.7 cells were stimulated for 18 hrs with 105 to 107 CFU/mL inocula of either of two prototypical community-acquired- (CA-) MRSA isolates, USA300 strain LAC and USA400 strain MW2. Then we added the NMDA inhibitors ketamine or 2R-amino-5-phosphonopentanoate (AP5), NMDA substrate, LY294002, and rapamycin in various combinations. Results. NMDA inhibition suppressed TNF secretion by almost a third compared to the no-ketamine control. When NMDA substrate was added, the TNF secretion increased by 10%. Addition of LY294002 suppressed TNF production by macrophages by 20%. Rapamycin exhibited a concentration-dependent TNF induction-suppression response: induction at doses of 0.1 and 1 ng/mL and suppression at 10 and 100 ng/mL. Induction of TNF was abolished when LY294002 was added and the suppression became uniform. Ketamine-induced suppression of TNF secretion was intensified 10–15% when rapamycin was added, but not when LY294002 was added. Conclusion. These findings suggest that NMDA-induced TNF suppression can be augmented by concurrent mTOR inhibition.
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spelling doaj-art-ed3572e6d9ee4df4a441d0895e665ea82025-08-20T02:22:09ZengWileyInternational Journal of Inflammation2090-80402042-00992012-01-01201210.1155/2012/542727542727Rapamycin Augments the NMDA-Mediated TNF Suppression of MRSA-Stimulated RAW264.7 Murine MacrophagesThomas Spentzas0Rebekah K. H. Shappley1Fabio Savorgnan2Elizabeth Meals3B. Keith English4Division of Pediatric Critical Care, Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38103, USADivision of Pediatric Critical Care, Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38103, USADivision of Pediatric Critical Care, Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38103, USAChildren's Foundation Research Center, Memphis, TN 38103, USAChildren's Foundation Research Center, Memphis, TN 38103, USABackground. Methicillin-resistant Staphylococcus aureus (MRSA) can stimulate massive cytokine release. Ketamine suppresses tumor necrosis factor (TNF) secretion by MRSA-stimulated RAW264.7 macrophages, and the mechanism likely involves N-methyl-D-aspartic acid (NMDA) receptor antagonism. The downstream effects of NMDA-mediated TNF suppression, specifically the PI3K/Akt and mTOR modulation, have not been described. Methods. RAW264.7 cells were stimulated for 18 hrs with 105 to 107 CFU/mL inocula of either of two prototypical community-acquired- (CA-) MRSA isolates, USA300 strain LAC and USA400 strain MW2. Then we added the NMDA inhibitors ketamine or 2R-amino-5-phosphonopentanoate (AP5), NMDA substrate, LY294002, and rapamycin in various combinations. Results. NMDA inhibition suppressed TNF secretion by almost a third compared to the no-ketamine control. When NMDA substrate was added, the TNF secretion increased by 10%. Addition of LY294002 suppressed TNF production by macrophages by 20%. Rapamycin exhibited a concentration-dependent TNF induction-suppression response: induction at doses of 0.1 and 1 ng/mL and suppression at 10 and 100 ng/mL. Induction of TNF was abolished when LY294002 was added and the suppression became uniform. Ketamine-induced suppression of TNF secretion was intensified 10–15% when rapamycin was added, but not when LY294002 was added. Conclusion. These findings suggest that NMDA-induced TNF suppression can be augmented by concurrent mTOR inhibition.http://dx.doi.org/10.1155/2012/542727
spellingShingle Thomas Spentzas
Rebekah K. H. Shappley
Fabio Savorgnan
Elizabeth Meals
B. Keith English
Rapamycin Augments the NMDA-Mediated TNF Suppression of MRSA-Stimulated RAW264.7 Murine Macrophages
International Journal of Inflammation
title Rapamycin Augments the NMDA-Mediated TNF Suppression of MRSA-Stimulated RAW264.7 Murine Macrophages
title_full Rapamycin Augments the NMDA-Mediated TNF Suppression of MRSA-Stimulated RAW264.7 Murine Macrophages
title_fullStr Rapamycin Augments the NMDA-Mediated TNF Suppression of MRSA-Stimulated RAW264.7 Murine Macrophages
title_full_unstemmed Rapamycin Augments the NMDA-Mediated TNF Suppression of MRSA-Stimulated RAW264.7 Murine Macrophages
title_short Rapamycin Augments the NMDA-Mediated TNF Suppression of MRSA-Stimulated RAW264.7 Murine Macrophages
title_sort rapamycin augments the nmda mediated tnf suppression of mrsa stimulated raw264 7 murine macrophages
url http://dx.doi.org/10.1155/2012/542727
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