Evaluation of lipopolysaccharide-induced activation of equine neutrophils.
OBJECTIVE
To evaluate lipopolysaccharide (LPS)-induced activation of equine neutrophils in blood.


METHODS
Blood samples from 5 healthy adult Thoroughbreds.


METHODS
Neutrophil integrin (CD11/CD18) expression, size variation, degranulation, and deformability were measured with and without incubation with LPS. Time and concentration studies were done. The mechanism of endotoxin-induced neutrophil activation was investigated by inactivating complement or preincubating neutrophils with inhibitors of tumor necrosis factor-alpha (TNF-alpha) synthesis, prostaglandin-leukotriene synthesis, or platelet-activating factor.


RESULTS
Incubation of equine neutrophils with LPS increased cell surface expression of CD11/CD18, decreased neutrophil deformability, increased and decreased neutrophil size, and induced neutrophil degranulation. The LPS-induced neutrophil activation was attenuated by addition of inhibitors of TNF-alpha and prostaglandin-leukotriene synthesis.


CONCLUSIONS
Equine neutrophils are readily activated in vitro by LPS, resulting in increased expression of integrin adhesion molecules, decreased deformability, variation in neutrophil size, and degranulation. The tests used to detect activated neutrophils in this study may be useful in detecting in vivo neutrophil activation in horses with sepsis and endotoxemia.
Weiss
Douglas J
DJ
Department of Veterinary PathoBiology, College of Veterinary Medicine, University of Minnesota, St Paul 55108, USA.
Evanson
Oral A
OA
D015117:5,8,11,14-Eicosatetraynoic Acid / Q000494:pharmacology; D000818:Animals; D001381:Azepines / Q000494:pharmacology; D018845:CD11 Antigens / Q000096:biosynthesis; D018821:CD18 Antigens / Q000096:biosynthesis; D015550:Cell Degranulation / Q000276:immunology; D003165:Complement System Proteins / Q000276:immunology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005434:Flow Cytometry / Q000662:veterinary; D006736:Horses / Q000097:blood / Q000276:immunology*; D016209:Interleukin-8 / Q000037:antagonists & inhibitors / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology / Q000494:pharmacology*; D018375:Neutrophil Activation / Q000187:drug effects* / Q000276:immunology; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D010431:Pentoxifylline / Q000494:pharmacology; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors / Q000276:immunology; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D014230:Triazoles / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000276:immunology
D001381:Azepines; D018845:CD11 Antigens; D018821:CD18 Antigens; D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D016209:Interleukin-8; D008070:Lipopolysaccharides; D010972:Platelet Activating Factor; D010975:Platelet Aggregation Inhibitors; D014230:Triazoles; D014409:Tumor Necrosis Factor-alpha; C433788:lipopolysaccharide, E. coli O26-B6; C052518:WEB 2086; D015117:5,8,11,14-Eicosatetraynoic Acid; D003165:Complement System Proteins; D010431:Pentoxifylline