Gallic acid reduces the effect of LPS on apoptosis and inhibits the formation of neutrophil extracellular traps

Gabriela Viegas Haute, Eduardo Caberlon, Eamim Squizani, Fernanda Cristina de Mesquita, Leonardo Pedrazza, Bianca Andrade Martha, Denizar Alberto da Silva Melo, Eduardo Cassel, Rafael Sanguinetti Czepielewski, Shanna Bitencourt, Márcia Inês Goettert, Jarbas Rodrigues de Oliveira

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)309-317
Number of pages9
JournalToxicology in Vitro
Volume30
Issue number1
DOIs
StatePublished - Dec 25 2015

Keywords

  • Apoptosis
  • Gallic acid
  • Inflammation
  • NETosis
  • Neutrophils
  • ROS

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