LFA-1/ICAM-3 mediates neutrophil homotypic aggregation under fluid shear stress.
We found that human neutrophils undergo homotypic aggregation by loading the physiological range of fluid shear stress (12-30 dynes/cm2). Under the fluid shear stress, an increase of intracellular Ca2+ concentration of neutrophils was observed. This increase of intracellular Ca2+ concentration was caused by Ca2+ influx, and the blockage of the flux by NiCl2 suppressed the neutrophil homotypic aggregation. Furthermore, this neutrophil aggregation under fluid shear stress was completely inhibited by pretreatment with antibody against LFA-1 or ICAM-3. These results suggested that NiCl2-sensitive Ca2+ channel played an important role in LFA-1/ICAM-3-mediated neutrophil homotypic aggregation under fluid shear stress.
Okuyama
M
M
Department of Surgery II, Osaka University Medical School, Japan.
Kambayashi
J
J
Sakon
M
M
Monden
M
M
D015703:Antigens, CD; D000943:Antigens, Differentiation; D002138:Calibration; D015815:Cell Adhesion Molecules / Q000276:immunology*; D002449:Cell Aggregation / Q000187:drug effects / Q000276:immunology; D005404:Fixatives; D005976:Glutaral; D006801:Humans; D016169:Lymphocyte Function-Associated Antigen-1 / Q000276:immunology*; D008863:Microspheres; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology*; D011134:Polysaccharides / Q000494:pharmacology; D013314:Stress, Mechanical
D015703:Antigens, CD; D000943:Antigens, Differentiation; D015815:Cell Adhesion Molecules; D005404:Fixatives; C483616:ICAM3 protein, human; D016169:Lymphocyte Function-Associated Antigen-1; D011134:Polysaccharides; C007789:fucoidan; D005976:Glutaral