Local inflammation, lethality and cytokine release in mice injected with Bothrops atrox venom

• Published in: Mediators of Inflammation Vol. 1998; no. 5; pp. 339 - 346
• Main Authors: Barros, S F, Friedlanskaia, I, Petricevich, V L, Kipnis, T L
• Format: Journal Article
• Language: English
• Published: United States Hindawi Limiteds 01.01.1998; Wiley
• Subjects: Animal venoms; Animals; Antibodies, Monoclonal - pharmacology; Bothrops; Bothrops a trox; Connective Tissue - drug effects; Connective Tissue - immunology; Connective Tissue - pathology; Crotalid Venoms - antagonists & inhibitors; Crotalid Venoms - immunology; Crotalid Venoms - toxicity; Cytokines; Cytokines - blood; Cytokines - secretion; Hemorrhage - prevention & control; Inflammation - chemically induced; Interferon-gamma - secretion; Interleukin-10 - secretion; Interleukin-6 - secretion; Lethal Dose 50; Male; Mediators of inflammation; Mice; Mice, Inbred BALB C; Mice, Inbred Strains; Nitric Oxide - biosynthesis; Species Specificity; Tumor Necrosis Factor-alpha - secretion; Cytokines; Animal venoms; Mediators of inflammation; Bothrops atrox
• ISSN: 0962-9351; 1466-1861
• DOI: 10.1080/09629359890866

WE have provided evidence that: (a) lethality of mice to crude Bothrops venom varies according the isogenic strain (A/J ＞ C57Bl/6 ＞ A/Sn ＞ BALB/c ＞ C3H/ HePas ＞ DBA/2 ＞ C3H/He); (b)BALB/c mice (LD_(50)=100.0 μg) were injected i.p. with 50 μg of venom produced IL-6, IL-10, INF-γ, TNF-α and NO in the serum. In vitro the cells from the mice injected and challenged with the venom only released IL-10 while peritoneal macrophages released IL-10, INF-γ and less amounts of IL-6; (c) establishment of local inflammation and necrosis induced by the venom, coincides with the peaks of TNF-α, IFN-γ and NO and the damage was neutralized when the venom was incubated with a monoclonal antibody against a 60 kDa haemorrhagic factor. These results suggest that susceptibility to Bothrops a trox venom is genetically dependent but MHC independent; that IL-6, IL10, TNF-α, IFN-γ and NO can be involved in the mediation of tissue damage; and that the major venom component inducers of the lesions are haemorrhagins.