Pretreatment of mice with lipopolysaccharide (LPS) or IL-1β exerts dose-dependent opposite effects on Shiga toxin-2 lethality
| Autor: | Gabriela C. Fernández, Carolina Rubel, Martín A. Isturiz, F. Alberto, M. Rivas, F. Alves-Rosa, G. Fernández-Alonso, Marina S. Palermo |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Lipopolysaccharides
Male medicine.medical_specialty Lipopolysaccharide medicine.medical_treatment Bacterial Toxins Immunology Dose-Response Relationship Immunologic Inflammation Biology Shiga Toxins Proinflammatory cytokine Mice chemistry.chemical_compound In vivo hemic and lymphatic diseases Internal medicine Escherichia coli medicine Animals Humans Immunology and Allergy Child Escherichia coli Infections Mice Inbred BALB C Tumor Necrosis Factor-alpha Immunity to Infection Shiga toxin Recombinant Proteins Disease Models Animal Endocrinology Cytokine chemistry Hemolytic-Uremic Syndrome Toxicity biology.protein Female Tumor necrosis factor alpha Inflammation Mediators medicine.symptom Corticosterone Interleukin-1 |
| Zdroj: | Clinical and Experimental Immunology. 119:77-83 |
| ISSN: | 1365-2249 0009-9104 |
| DOI: | 10.1046/j.1365-2249.2000.01103.x |
| Popis: | SUMMARY Haemolytic uraemic syndrome (HUS) has been closely associated with infection with a group of Shiga toxin-producing enterohaemorrhagic Eschericchia coli in young children. Shiga toxins (Stx) have been implicated as pathogenic agents of HUS by binding to the surface receptor of endothelial cells. LPS is a central product of the Gram-negative bacteria and several reports have documented that both LPS and Stx are important for disease development. In this study the reciprocal interactions between LPS and Stx2 are analysed in a mouse model. The results demonstrated that LPS was able to reduce or enhance Stx2 toxicity, depending on the dose and the timing of the injection. The involvement of the main early cytokines induced by LPS, tumour necrosis factor alpha (TNF-α) and IL-1β, in those LPS opposite effects on Stx2 toxicity was evaluated. Stx2 toxicity was enhanced by in vivo injection of murine TNF-α and low doses of murine IL-1β. However, at higher doses of IL-1β which induced corticosteroid increase in serum, Stx2 lethality was decreased. Considering that dexamethasone and IL-1β reproduce the LPS protective effects, it is suggested that endogenous corticosteroids secondary to the inflammatory response induced by LPS, mediate the protection against Stx2. It can be concluded that the fine equilibrium between proinflammatory and anti-inflammatory activities strongly influences Stx2 toxicity. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|