Thalidomide inhibits granulocyte responses in healthy humans after ex vivo stimulation with bacterial antigens.
Ingestion of thalidomide was associated with a reduction in the upregulation of the granulocyte activation marker CD11b and a reduced capacity to release elastase and lactoferrin after stimulation with lipopolysaccharide or lipoteichoic acid. A single oral dose of thalidomide attenuates neutrophil activation upon ex vivo stimulation with bacterial antigens.
Juffermans
N P
NP
Laboratory of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Verbon
A
A
Schultz
M J
MJ
Hack
C E
CE
van Deventer
S J
SJ
Speelman
P
P
van der Poll
T
T
D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000942:Antigens, Bacterial / Q000494:pharmacology*; D004347:Drug Interactions; D006098:Granulocytes / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D007781:Lactoferrin / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D016177:Macrophage-1 Antigen / Q000378:metabolism*; D018375:Neutrophil Activation / Q000187:drug effects*; D010196:Pancreatic Elastase / Q000378:metabolism; D013792:Thalidomide / Q000494:pharmacology*
D000893:Anti-Inflammatory Agents; D000942:Antigens, Bacterial; D008070:Lipopolysaccharides; D016177:Macrophage-1 Antigen; D013792:Thalidomide; D007781:Lactoferrin; D010196:Pancreatic Elastase