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Short term incubation of bovine neutrophils with Escherichia coli lipopolysaccharide increases their production of reactive oxygen species and formation of extracellular traps in a dose‐dependent manner but has no effect on their chemotactic and antimicrobial capacities
Author(s) -
Revelo Xavier,
Waldron Matthew
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.752.1
Subject(s) - lipopolysaccharide , nadph oxidase , reactive oxygen species , intracellular , escherichia coli , extracellular , neutrophil extracellular traps , chemotaxis , chemistry , staphylococcus aureus , incubation , neutrophile , microbiology and biotechnology , biochemistry , biology , receptor , inflammation , bacteria , in vitro , immunology , genetics , gene
The objective of this study was to investigate the effects of Escherichia coli lipopolysaccharide (LPS) on the function of blood neutrophils (PMNL) harvested from Holstein cows (n = 7). PMNL were incubated with 0, 1, 25 and 50 μg/mL of LPS for 120 min and the generation of reactive oxygen species (ROS), formation of extracellular traps (NETs), chemotactic and antimicrobial capacities were determined. LPS increased the total and intracellular production of ROS in a dose‐dependent manner. Areas under the curves indicated that 50 μg/mL of LPS enhanced intracellular ROS in non‐stimulated PMNL by 184% whereas 25 and 50 μg/mL of LPS increased intracellular ROS in stimulated cells by 79 and 145%, respectively. These effects were partially inhibited by diphenyleneiodonium chloride, a NADPH oxidase blocker. Treatment of neutrophils with 25 and 50 μg/mL of LPS resulted in a 105% increase of NETs release by non‐stimulated PMNL. LPS had no effect on PMNL chemotaxis and did not alter their capacity to kill Staphylococcus aureus . These results suggest that LPS “primes” the neutrophils toward enhanced immunity by increasing the generation of ROS and the expression of NETs. Internal funds.