TY - JOUR
T1 - Gallic acid reduces the effect of LPS on apoptosis and inhibits the formation of neutrophil extracellular traps
AU - Haute, Gabriela Viegas
AU - Caberlon, Eduardo
AU - Squizani, Eamim
AU - de Mesquita, Fernanda Cristina
AU - Pedrazza, Leonardo
AU - Martha, Bianca Andrade
AU - da Silva Melo, Denizar Alberto
AU - Cassel, Eduardo
AU - Czepielewski, Rafael Sanguinetti
AU - Bitencourt, Shanna
AU - Goettert, Márcia Inês
AU - de Oliveira, Jarbas Rodrigues
N1 - Funding Information:
This study was supported by CNPq ( 143969/2013-7 ). G.V.H. received a fellowship from PUCRS. S.B. is the recipient of a PNPD/Capes postdoc grant from CAPES -Brazil.
Publisher Copyright:
© 2015 Elsevier Ltd.
PY - 2015/12/25
Y1 - 2015/12/25
N2 - Apoptosis and NETosis of neutrophils are two major mechanisms of programmed cell death that differ in their morphological characteristics and effects on the immune system. Apoptosis can be delayed by the presence of pathogens or chemical components such as lipopolysaccharide (LPS). Neutrophils have other antimicrobial strategy, called neutrophil extracellular traps (NETs), which contributes to the elimination and control of the pathogen. NETosis is induced by infection, inflammation or trauma and represents an innate immune activation mechanism. The objective of this study was to evaluate the effect of gallic acid (GA) in the modulation of apoptosis and NETs release. The results show that GA decreased the anti-apoptotic effect of LPS, blocked the induction of NETs and prevented the formation of free radicals induced by LPS. These findings demonstrate that the GA is a novel therapeutic agent for decreasing the exacerbated response of the body against an infectious agent.
AB - Apoptosis and NETosis of neutrophils are two major mechanisms of programmed cell death that differ in their morphological characteristics and effects on the immune system. Apoptosis can be delayed by the presence of pathogens or chemical components such as lipopolysaccharide (LPS). Neutrophils have other antimicrobial strategy, called neutrophil extracellular traps (NETs), which contributes to the elimination and control of the pathogen. NETosis is induced by infection, inflammation or trauma and represents an innate immune activation mechanism. The objective of this study was to evaluate the effect of gallic acid (GA) in the modulation of apoptosis and NETs release. The results show that GA decreased the anti-apoptotic effect of LPS, blocked the induction of NETs and prevented the formation of free radicals induced by LPS. These findings demonstrate that the GA is a novel therapeutic agent for decreasing the exacerbated response of the body against an infectious agent.
KW - Apoptosis
KW - Gallic acid
KW - Inflammation
KW - NETosis
KW - Neutrophils
KW - ROS
UR - http://www.scopus.com/inward/record.url?scp=84958679398&partnerID=8YFLogxK
U2 - 10.1016/j.tiv.2015.10.005
DO - 10.1016/j.tiv.2015.10.005
M3 - Article
C2 - 26475966
AN - SCOPUS:84958679398
VL - 30
SP - 309
EP - 317
JO - Toxicology in Vitro
JF - Toxicology in Vitro
SN - 0887-2333
IS - 1
ER -