RAGE KO mice were partially protected from lung damage caused by S. aureus pneumonia, whereas TLR4 KO mice were not protected at all.
In conclusion, the analysis of early molecular biomarkers provided evidence that oral metformin is able to protect the mouse lung from MCS-induced DNA damage and to modulate a variety of miRNAs involved in pulmonary carcinogenesis.
TS can cause DNA damage in mouse lung cells by facilitating the formation of chemical cross-links between DNA and proteins, an event that can be prevented by VE supplementation in this study.
In fact, many studies implicate neutrophils or neutrophil-like cells, and chemokines that recruit neutrophils, as causal mediators of lung damage in mice (Keller et al., 2006; Lyadova et al., 2010; Nandi and Behar, 2011; Yang et al., 2012; Gopal et al., 2013; Major et al., 2013; Dorhoi et al., 2014; Nouailles et al., 2014).
This study was designed to evaluate the anti-inflammatory and anti-fibrotic effect of thalidomide on PQ-induced lung damage in a mouse model.
Dietary FS given post-XRT mitigates radiation effects by decreasing pulmonary fibrosis, inflammation, cytokine secretion and lung damage while enhancing mouse survival.
Furthermore, these studies identified macrophage elastase (matrix metalloproteinase 12 (MMP12)) as an additional protease contributing to early lung damage in βENaC-Tg mice.
Fig. 1 Neutrophil elastase (NE) and matrix metalloproteinase 12 (MMP12) activity is increased at the surface of bronchoalveolar neutrophils and macrophages and is associated with structural lung damage in βENaC-Tg mice.
Although there was no increased lung damage in Mmp8−/− mice, and the role of inflammation in idiopathic fibrosis is discussed, this could be a relevant side effect.
This suggests reduction in lung damage in CCR2−/− mice may be due to reduced TRAIL ligand availability.
