Andrade Marcus V, Lisboa Felipe Assis, Portugal André Lopes, Arantes Rosa Maria Esteves, Cunha-Melo José Renan
Department of Internal Medicine, School of Medicine, Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, MG 30130-100, Brazil.
Comp Biochem Physiol A Mol Integr Physiol. 2007 Apr;146(4):581-7. doi: 10.1016/j.cbpa.2006.01.031. Epub 2006 Mar 31.
Previous studies have demonstrated that scorpion toxins increase the serum levels of IL-1, IL-6, INF-gamma, and GM-CSF in patients with severe shock and pulmonary edema. Moreover, it has been shown that experimental models of scorpion envenomation presented an increase in serum levels of IL-1, IL-6, IFN-gamma and nitric oxide. Thus, it is possible that the cytokine release may contribute to the onset and maintenance of the pulmonary edema induced by scorpion venom. This study was designed to investigate whether inflammatory and non-inflammatory cytokines, contribute to the pulmonary injury induced by infusion of Tityus serrulatus scorpion toxin in rats. We show that scorpion venom not only increases the expression of mRNA pulmonary inflammatory cytokines but also non-inflammatory cytokines as well. Moreover, the expression of IL-1alpha, IL-1beta and IL-6 mRNA was shown to be higher among the remaining detectable cytokines. The findings of this study provide additional insight towards the understanding of the pathophysiology of the pulmonary edema induced by scorpion venom. The increased level of pulmonary cytokines observed during the pulmonary edema may be responsible for the exacerbation and maintenance of the inflammatory response to scorpion venom in the lungs.
先前的研究表明,蝎子毒素会使严重休克和肺水肿患者的白细胞介素-1(IL-1)、白细胞介素-6(IL-6)、γ干扰素(INF-γ)和粒细胞-巨噬细胞集落刺激因子(GM-CSF)血清水平升高。此外,研究显示蝎子蜇伤的实验模型中,IL-1、IL-6、γ干扰素(IFN-γ)和一氧化氮的血清水平有所升高。因此,细胞因子的释放可能促使了蝎子毒液诱发肺水肿的发生和持续。本研究旨在调查炎性和非炎性细胞因子是否会导致大鼠输注锯齿脂鲤属蝎子毒素引发的肺损伤。我们发现蝎子毒液不仅会增加肺部炎性细胞因子的mRNA表达,还会增加非炎性细胞因子的表达。此外,白细胞介素-1α(IL-1α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的mRNA表达在其余可检测的细胞因子中更高。本研究结果为理解蝎子毒液诱发肺水肿的病理生理学提供了更多见解。肺水肿期间观察到的肺部细胞因子水平升高,可能是肺部对蝎子毒液炎症反应加剧和持续的原因。