There are about 1,500 scorpion species in nature. From these species, about 50 have venom toxic to humans. Poisoning by scorpion cause local symptoms in the bite region as intense pain and redness, and can induce very relevant systemic manifestations. Among the most important clinical manifestations include the acute pulmonary edema, cardiogenic shock, which can lead to death. However, mediators and other factors responsible for cardiac manifestations are little known. In recent years we have studied the mechanisms that lead to inflammation and pulmonary edema in scorpionism. We demonstrated that venom of the scorpion Tityus serrulatus (native of Brazil and present in large urban centers) is recognized for venom-associated molecular pattern (VAMPS) resulting in rapid and massive release of several pro-inflammatory cytokines such as IL-1², IL 6, IL-8 and TNF-±, and eicosanoids. The cytokines and eicosanoids (especially prostaglandin E2 (PGE2)) in the lungs, via cAMP, induces the activation of NF-kB, amplifying inflammasome activation, and therefore the massive production of IL-1². IL-1² and PGE2 induce severe pulmonary edema, thereby exacerbating the patient's condition. As mentioned above, the mechanisms that lead to cardiogenic shock are not completely understood but it is known that release of pro-inflammatory cytokines, vasoactive peptides and the venom thrombogenic peptides act in coronary arteries facilitating platelet aggregation and thrombus formation. In this project, we will initially investigate in vitro cells, and then in mice, like the scorpion venom, via cytokines and eicosanoids, participate in cardiogenic shock. We hope to find a new tool that prevents or improves cardiac changes that occur in the scorpionism.
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