TY - JOUR
T1 - Cardiac gene expression and function in a mouse model of community-acquired methicillin-resistant Staphylococcus aureus sepsis
T2 - Role of inflammatory caspases 1 and 11
AU - Hume, Janet R.
AU - Zhang, Yuan
AU - Zhang, Lei
AU - Peterson, Marnie
AU - Carlson, Deborah L.
N1 - Funding 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.
Publisher Copyright:
© The Author(s) 2019.
PY - 2019
Y1 - 2019
N2 - 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.
AB - 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.
KW - cardiomyopathy
KW - caspase 1
KW - caspase 11
KW - inflammasome
KW - sepsis
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U2 - 10.1177/2058739219838389
DO - 10.1177/2058739219838389
M3 - Letter
AN - SCOPUS:85081411518
SN - 1721-727X
VL - 17
JO - European Journal of Inflammation
JF - European Journal of Inflammation
ER -