Table 1.
Implications of cell-specific GR deletion on sepsis progression.
| Tissue/cell | GR deletion | Effect of GR deletion in sepsis model | References |
|---|---|---|---|
| Liver | shRNA-GR | Excessive liver and systemic inflammation Increased mortality (CLP) |
(34) |
| IEC | Villin cre | Increased ISG expression in gut, intestinal permeability Increased mortality (LPS, TNF) |
(35, 36) |
| Skeletal and cardiac muscle | Mck cre | Reduced muscle atrophy (LPS) | (37) |
| Vascular smooth muscle | SM22-α cre | Small trend toward increased mortality (LPS) | (38) |
| Endothelial cell | Tie-1 cre | Hemodynamic instability, higher NO levels, excessive systemic inflammation Increased mortality (LPS) |
(38) |
| Myeloid cells/macrophages | LysM cre | Excessive systemic inflammation, ALI Increased mortality (LPS) |
(36, 39–41) |
| Thymocytes/T-cells | Lck cre | Resistance to CLP-induced thymocyte apoptosis Increased mortality (CLP) |
(42) |
| DCs | CD11c cre | Excessive systemic inflammation (IL-12) Increased mortality (LPS) |
(43) |
| NK cells | Ncr1 cre | Increased IFN-γ production, spleen immunopathology Increased mortality (CMV, LPS) |
(44, 45) |
IEC, intestinal epithelial cell; CLP, cecal ligation and puncture; LPS, lipopolysaccharide; TNF, tumor necrosis factor; ISG, interferon-stimulated genes; NO, nitric oxide; ALI, acute lung injury; DC, dendritic cell; NK, natural killer; CMV, cytomegalovirus.