Evaluation of the susceptibility to fipronil of Rhipicephalus microplus larvae from egg masses incubated at different times of oviposition.

The objective of this work was to evaluate the susceptibility of R. microplus larvae from different oviposition times to fipronil. The LPT was performed in sextuplicate, at concentrations of 18.75, 37.5, 75, 150 and 300 µg.mL-1. The LC50 found for the egg masses incubated with +7, +14 and +21 days were respectively 105.87, 110.71 and 121.22 µg.mL-1. The larvae originating from egg masses from the same group of engorged females, incubated on different days, presented similar mortality rates compared to the evaluated fipronil concentrations, facilitating the maintenance of laboratory colonies of this tick species.

O objetivo deste trabalho foi avaliar a susceptibilidade de larvas de R. microplus oriundas de diferentes momentos da oviposição frente ao fripronil. O TPL foi realizado em sextuplicata, nas seguintes concentrações 18,75; 37,5; 75; 150; 300 µg.mL-1. Não houve diferença estatística entre as mortalidades das larvas oriundas de posturas incubadas nos dias mais sete, +14 e +21, expostas ao fipronil. As CL50 encontradas para as posturas incubadas com +7, +14 e +21 dias foram respectivamente 105,87; 110,71 e 121,22 µg.mL-1. Observou-se que as larvas oriundas de posturas, do mesmo grupo de fêmeas ingurgitadas, incubadas em dias diferentes apresentam taxas de mortalidade parecidas frente as concentrações de fipronil avaliadas, facilitando a manutenção das colônias laboratorias desta espécie de carrapato.

A Metabolic Shift toward Pentose Phosphate Pathway Is Necessary for Amyloid Fibril- and Phorbol 12-Myristate 13-Acetate-induced Neutrophil Extracellular Trap (NET) Formation.

Neutrophils are the main defense cells of the innate immune system. Upon stimulation, neutrophils release their chromosomal DNA to trap and kill microorganisms and inhibit their dissemination. These chromatin traps are termed neutrophil extracellular traps (NETs) and are decorated with granular and cytoplasm proteins. NET release can be induced by several microorganism membrane components, phorbol 12-myristate 13-acetate as well as by amyloid fibrils, insoluble proteinaceous molecules associated with more than 40 different pathologies among other stimuli. The intracellular signaling involved in NET formation is complex and remains unclear for most tested stimuli. Herein we demonstrate that a metabolic shift toward the pentose phosphate pathway (PPP) is necessary for NET release because glucose-6-phosphate dehydrogenase (G6PD), an important enzyme from PPP, fuels NADPH oxidase with NADPH to produce superoxide and thus induce NETs. In addition, we observed that mitochondrial reactive oxygen species, which are NADPH-independent, are not effective in producing NETs. These data shed new light on how the PPP and glucose metabolism contributes to NET formation.