| First Author | Sasaki S | Year | 2002 |
| Journal | Microb Pathog | Volume | 33 |
| Issue | 1 | Pages | 43-7 |
| PubMed ID | 12127799 | Mgi Jnum | J:102983 |
| Mgi Id | MGI:3608296 | Doi | 10.1006/mpat.2002.0509 |
| Citation | Sasaki S, et al. (2002) Roles of gamma interferon and tumor necrosis factor-alpha in shiga toxin lethality. Microb Pathog 33(1):43-7 |
| abstractText | Shiga toxins (Stxs) have been specifically implicated as a causal factor of hemolytic uremic syndrome and acute encephalopathy. The first step of Stx-induced brain damage is considered to injure endothelial cells cooperating with tumor necrosis factor-alpha (TNF-alpha). Gamma interferon (IFN-gamma) is one of the proinflammatory cytokines as well as TNF-alpha is critical in activation of endothelial cells. Therefore we focused on the possibility of IFN-gamma-mediated lethality of Stx1 or Stx2 in mice. All of mice died within 3-4 days after injection with 400 ng of Stx1 and 37.5% of mice, which had been injected with 133 ng, survived. In contrast, a lethal dose of Stx2 was 40 times lower than that of Stx1. When mice were given 400 ng of Stx1 or 10 ng of Stx2, IFN-gamma mRNA was detected in the spleens 24h after injection. Moreover, when mice were injected with 133 ng of Stx1 or 3.3 ng of Stx2, survival rates of IFN-gamma-deficient mice and TNF-alpha-deficient mice were significantly higher than that of wild-type mice. The present study using cytokine-gene knockout mice directly demonstrated that not only TNF-alpha but also IFN-gamma is involved in lethality of Stx1 and Stx2. |
