Knockout of MAPK Phosphatase-1 Exaggerates Type I IFN Response during Systemic Infection.

We have previously shown that -deficient mice produce elevated TNF-α, IL-6, and IL-10 following systemic infection, and they exhibited increased mortality, elevated bacterial burden, and profound metabolic alterations. To understand the function of Mkp-1 during bacterial infection, we performed RNA-sequencing analysis to compare the global gene expression between -infected wild-type and mice. A large number of IFN-stimulated genes were more robustly expressed in -infected mice than in wild-type mice.

Dysregulation of Lipid Metabolism in Mkp-1 Deficient Mice during Gram-Negative Sepsis.

Mitogen-activated protein kinase phosphatase (Mkp)-1 exerts its anti-inflammatory activities during Gram-negative sepsis by deactivating p38 and c-Jun N-terminal kinase (JNK). We have previously shown that mice, but not mice, exhibit hypertriglyceridemia during severe sepsis. However, the regulation of hepatic lipid stores and the underlying mechanism of lipid dysregulation during sepsis remains an enigma.