Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/338172
Type: Artigo
Title: BAY 41-2272 inhibits human neutrophil functions
Author: Rosa, Paola Vendramini Ferreira
Carvalho, Marina Uchoa Wall Barbosa de
Soeiro-Pereira, Paulo Vítor
Harumi, Renata Cruz
Albuquerque, Rafael Sales de
Antunes, Edson
Condino-Neto, Antonio
Abstract: BAY 41-2272 is a guanylyl cyclase (GC) stimulator derived from YC-1 (3-[(5′-hydroxymethyl-2′-furyl)-1-benzyl indazole]). Previous studies by our group showed that BAY 41-2272 activates human monocytes via soluble guanylyl cyclase (sGC) and cGMP. In this study, we investigated the effect of BAY 41-2272 on human neutrophil function and found that 30 μM BAY 41-2272 inhibits neutrophil migration (1.82-fold lower than FMLP, P < 0.05 by one-way ANOVA followed by Tukey's test), oxidative burst (1.70-fold lower than PMA, P < 0.05 by one-way ANOVA followed by Tukey's test), and IL-8 cytokine production (1.80-fold lower than PMA, P < 0.05 by one-way ANOVA followed by Tukey's test). Our results suggest that these effects are independent of the sGC pathway but dependent instead on cGMP production, as the response induced by 30 μM BAY 41-2272 was 6.40-fold greater than that observed in our negative control (P < 0.05 by parametric t-test). 1H-[1, 2, 4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ), which is an irreversible inhibitor of sGC, was unable to reverse the effects of BAY 41-2272 on human neutrophils, indicating that this drug acts independently of sGC. Our results confirm the immunomodulatory effect of BAY 41-2272 on human neutrophils
Subject: Neutrófilos
Fatores imunológicos
Country: Estados Unidos
Editor: Elsevier
Rights: Fechado
Identifier DOI: 10.1016/j.intimp.2019.105767
Address: https://www.sciencedirect.com/science/article/pii/S1567576918306556
Date Issue: Oct-2019
Appears in Collections:FCM - Artigos e Outros Documentos

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