Compared to wild-type mice, CXCR3-deficient mice show less systemic cytokine production, attenuated physiologic dysfunction and improved survival during severe sepsis caused by cecal ligation and puncture (CLP) [ 11].
Experimental models find that female mice show greater systemic resistance to pneumococci (Weiss et al., 1973; Kadioglu et al., 2011) and to many other (but not all) pathogens (McClelland and Smith, 2011).
However TgS100a8a9 hep mice showed a systemic enrichment of neutrophils without activation and site-specific recruitment.
We expected constitutively active IKKβ transgenic mice showed enhanced systemic and adipose tissue inflammation (Jiao et al., 2012).
Even more striking, Casp8ΔIEC mice showed a systemic spread of luminal bacteria into different organs suggesting that barrier defects in caspase-8-deficient mice might be responsible for the lethal outcome (figure 6B, C).
By using transgenic mice expressing human apoE3 or apoE4, Lynch et al. [14] determined that apoE4 mice showed elevated systemic and brain pro-inflammatory cytokines following intravenous administration of LPS, and Ophir et al. [12] demonstrated that the expression of inflammation genes was higher and more prolongated in the brains of apoE4 following intracerebroventricular injection of LPS.
Using the Zurich 1 PrPKO and matched wild type (Wt) mice expressing normal levels of PrP as experimental models, we demonstrate that PrPKO mice show a phenotype of systemic iron deficiency and altered iron homeostasis compared to Wt controls.
Consistently, p66Shc−/− mice show reduced levels of systemic (isoprostane) and tissue (nitrotyrosine, 8-oxo-dG) oxidative stress markers [ 68, 76, 77] and enhanced resistance to oxidative stress induced by hypercholesterolemia [ 78], angiotensin II [ 79], carbon tetrachloride, and ethanol [ 80].
Likewise, p66Shc-/ mice show diminished levels of both systemic (isoprostane) and intracellular (nytrotyrosines, 8-oxo-dG) oxidative stress [ 14, 18, 19].
