Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is an important cause of invasive infections, including sepsis associated with myocardial dysfunction. Caspases 1 and 11, involved in activation of the inflammasome, have been shown to be critical in response to sepsis as well as myocardial dysfunction of numerous etiologies. We examined the survival, myocardial function, and production of inflammatory mediators in mice lacking caspases 1 and 11. Cas 1/11 KO mice demonstrated no significant difference in mortality or in cardiac shortening fraction relative to control mice. Cas 1/11 KO mice had significantly reduced upregulation of expression of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in the heart relative to control mice after CA-MRSA infection, as well as reduced serum production of IL-1β, TNF-α, and IL-6, with no difference in IL-10 production. Other inflammatory mediators beyond IL-1β, TNF-α, and IL-6 may be involved in myocardial dysfunction in CA-MRSA sepsis.
|Original language||English (US)|
|Journal||European Journal of Inflammation|
|State||Published - 2019|
Bibliographical noteFunding Information:
The authors would like to acknowledge the technical assistance provided by Mohamed Elsheikh, who was supported by the Undergraduate Research Opportunities Program at the University of Minnesota. In addition, we would like to acknowledge Dr Elizabeth Braunlin for reading and commenting on this manuscript.
© The Author(s) 2019.
- caspase 1
- caspase 11