Investigation of cardiac changes that occur in poisoning by Tityus serrulatus scorpion venom

• Grant number: 17/02314-3
• Support Opportunities: Scholarships in Brazil - Doctorate
• Start date: December 01, 2017
• End date: March 31, 2020
• Field of knowledge: Health Sciences - Pharmacy - Toxicological Analysis
• Principal Investigator: Lúcia Helena Faccioli
• Grantee: Mouzarllem Barros dos Reis
• Host Institution: Faculdade de Ciências Farmacêuticas de Ribeirão Preto (FCFRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
• Associated research grant: 14/07125-6 - New functional aspects of eicosanoids, AP.TEM

Abstract

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.

Scientific publications

(4)

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

REIS, MOUZARLLEM B.; ELIAS-OLIVEIRA, JEFFERSON; PASTORE, MARCELLA R.; RAMOS, SIMONE G.; GARDINASSI, LUIZ G.; FACCIOLI, LUCIA H.. Interleukin-1 Receptor-Induced Nitric Oxide Production in the Pancreas Controls Hyperglycemia Caused by Scorpion Envenomation. TOXINS, v. 12, n. 3, MAR 2020. (17/02314-3, 14/07125-6)

REIS, MOUZARLLEM BARROS; ZOCCAL, KARINA FURLANI; GARDINASSI, LUIZ GUSTAVO; FACCIOLI, LUCIA HELENA. Scorpion envenomation and inflammation: Beyond neurotoxic effects. Toxicon, v. 167, p. 174-179, SEP 2019. (17/02314-3, 14/07125-6)

DOS REIS, MOUZARLLEM BARROS; FACCIOLI, LUCIA HELENA. CARDIAC DYSFUNCTION INDUCED BY SCORPION ENVENOMATION IS MEDIATED BY NLRP3-INDUCED ACUTE MYOCARDITIS. Toxicon, v. 168, p. 1-pg., 2019-10-05. (17/02314-3, 15/00658-1, 14/07125-6)

REIS, MOUZARLLEM B.; RODRIGUES, FERNANDA L.; LAUTHERBACH, NATALIA; KANASHIRO, ALEXANDRE; SORGI, CARLOS A.; MEIRELLES, ALYNE F. G.; SILVA, CARLOS A. A.; ZOCCAL, KARINA F.; SOUZA, CAMILA O. S.; RAMOS, SIMONE G.; et al. Interleukin-1 receptor-induced PGE(2) production controls acetylcholine-mediated cardiac dysfunction and mortality during scorpion envenomation. NATURE COMMUNICATIONS, v. 11, n. 1, OCT 28 2020. (15/21976-1, 14/07125-6, 17/02314-3, 15/00658-1)

Academic Publications

(References retrieved automatically from State of São Paulo Research Institutions)

REIS, Mouzarllem Barros dos. Investigation of cardiac alterations that occur in poisoning by Tityus serrulatus scorpion venom. 2020. Doctoral Thesis - Universidade de São Paulo (USP). Faculdade de Medicina de Ribeirão Preto (PCARP/BC) Ribeirão Preto.