Premium
Changed expression of leukocyte adhesion molecules and increased production of reactive oxygen species caused by Streptococcus pyogenes in human whole blood
Author(s) -
Saetre TORUNN,
HÖIby E. ARNE,
KÄHler HANNE,
Lyberg TORSTEIN
Publication year - 2000
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1034/j.1600-0463.2000.d01-99.x
Subject(s) - reactive oxygen species , streptococcus pyogenes , cell adhesion molecule , chemistry , nitric oxide , microbiology and biotechnology , integrin alpha m , whole blood , bacteria , immunology , immune system , biology , biochemistry , organic chemistry , genetics , staphylococcus aureus
To elucidate the innate immune responses to group A streptococci (GAS) important in the pathophysiology of sepsis, flow cytometric techniques were applied to study the effects of live and heat‐inactivated GAS, including their particulate and soluble components, on the expression of leukocyte adhesion molecules CDllb (Mac‐1) and CD62L (L‐selectin), and leukocyte production of reactive oxygen species (ROS) in human whole blood. GAS caused marked time‐ and concentration‐dependent increases in CD11b and ROS, while CD62L was downregulated. Live and heat‐inactivated GAS induced similar changes in leukocyte adhesion molecules, whereas ROS production induced by heat‐inactivated GAS (and its particulate fraction) was 4 (2.5)‐fold higher than with live GAS. Leukocyte nitric oxide production (24 h) was not enhanced. Although GAS proved a more potent inducer of ROS production, leukocyte responses to GAS were similar to those reported for lipolysaccharides, indicating that Gram‐positive and Gram‐negative bacteria activate common pathways in the inflammatory response. High ROS production may contribute to tissue damage caused by GAS.