Table 2.
Summary of renal disease induced by Shiga toxin (Stx) in mice.
| Reference | Toxin or bacterial strain | LPS | Mouse strain | Renal pathology |
|---|---|---|---|---|
| [18,30] | E. coli O157:H7 orally | No | CD-1 | Bilateral renal cortical necrosis Glomeruli normal by light and electron microscopy |
| [31] | Stx-1, 0·01–2 µg intraperitoneally | E. coli O155:B8 | C3H/HeN | Mild to severe tubular injury with increasing Stx dose Tubular injury enhanced by administration of either LPS or TNF-α No glomerular abnormalities: no microvascular thrombosis |
| [23] | Stx-1 or Stx-2 1 µg–100 pg | None | CD-1 | Renal tubular damage greater in Stx-2 compared with Stx-1 treated mice |
| [29] | E. coli O157:H7 intragastrically | None | C3H/HeN (LPS-responder) C3H/HeJ (LPS non-responder) | Focal proliferation of mesangial cells and increased mesangial matrix. Tubular cell necrosis. No glomerular thrombi Renal histology did not differ between LPS-responder and LPS-non-responder mice |
| [20] | Purified Stx-2 250 pg intravenously | E. coli O111:B4 | BALB/c | Vascular congestion, diffuse interstitial inflammation, tubular cell necrosis |
| [21] | Purified Stx-2 600 pg intravenously | E. coli O111:B4 | BALB/c | Major lesions in cortical tubules No evidence of thrombi or renal microangiopathy |
| [33] | Purified Stx-1 500 pg intravenously | None | BALB/c | Moderate to severe widespread glomerular mesangial hypercellularity and crescent formation Treatment of mice with nitric oxide inhibitor resulted in PAS-positive amorphous material in the glomerular tufts consistent with thrombosis |
| [22] | Purified Stx-1 and Stx-2 1·5–4× LD50 | None | BALB/c | Tubular necrosis Glomerular morphology was normal |
| [32] | Purified Stx-1 50–100× LD50 intraperitoneally | None | BALB/c | Tubular dilatation and tubular cell apoptosis |
| [25] | Purified Stx-2 200 ng intraperitoneally | LPS (subtype not reported) | C3H/HeN | Focal proliferation of mesangial cells and infiltration of neutrophils Electron microscopy showed focal endothelial cell detachment, mild glomerular endothelial swelling and increased subendothelial space |
| [24] | Purified Stx-2 200–250 pg/g intravenously | None | ADAMTS13-deficient mice on (129/Sv × C57BL/6) or CASA/Rk genetic background | No disease in (129/Sv × C57BL/6) Adamts13−/− mice CASA/Rk Adamts13−/− mice developed red cell fragments on blood film, widespread vWF-rich, fibrin-poor thrombi in small vessels of multiple organs including kidney. Changes were consistent with thrombotic thrombocytopenic purpura |
| [27] | Purified Stx-2 225 ng/kg intraperitoneally | E. coli O55:B5 | C57Bl/6 | Glomerular red cell congestion and fibrin deposition Red cell and fibrin thrombi seen in glomerular arterioles Electron microscopy showed red cell congestion and electron-dense flocculent material and podocyte swelling |
| [26] | Purified Stx-2 4–12 ng intraperitoneally | E. coli O55:B5 | C57Bl/6 | Glomerular congestion with dilated capillary tufts filled with red cells and neutrophils |
aWF, von Willebrand factor; E. coli, Escherichia coli; LD50, lethal dose 50%; LPS, lipopolysaccharide; PAS, periodic acid-Schiff; TNF, tumour necrosis factor.