Characterization of Influenza Virus-Induced Leukocyte Adherence to Human Umbilical Vein Endothelial Cell Monolayers
ARMED FORCES RADIOBIOLOGY RESEARCH INST BETHESDA MD
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The adherence of undifferentiated Cr-labeled HL-60 0.5 x106 HL-60 cellswell cells was monitored on influenza virus-infected HUVEC monolayers. Whereas only 3.0 -- 1.6 n 36 of HL-60 cells adhered to uninfected HUVEC, adherence was increased to 41.7 -- 2.2 n 6, 79.7 - 1.2 n 6, 83.9 - 0. 7 n 6, and 84.4 or - 0.5 n 6 on HUVEC infected for 7 h at a MOI of 1, 3, 6, and 9, respectively. In comparison, HL-60 cell adherence increased to 35 when HUVEC monolayers were stimulated with LPS 0.2-20 microns for 4 h. Increased adherence to infected HUVEC occurred at 5 h postinfection, peaked at 7 h, and was maintained at 24 h postinfection. Active virus and metabolically active endothelial cells were required to mediate the virus-induced adherence. E-selectin and ICAM-1 Ag were upregulated 78.3- and 4.1 -fold, respectively, by LPS 0.02-20 microns, 4 h whereas virus infection 7 h only increased these proteins 2.6- and 1.4-fold with a MOI approx. 16. Although the time courses of expression for both adhesion molecules after LPS treatment or virus infection were similar, the difference in the magnitude of upregulation suggests that virus-induced adherence is not a result of upregulation of E-selectin and ICAM- 1. In contrast, surface expression of HA is involved in HL-60 cell adherence to virus-infected HUVEC because 1 the time course and magnitude of HA Ag expression paralleled the time course and magnitude of HL-60 cell adherence after virus infection of HUVEC 2 HL-60 cell aggregates were absent on infected HUVEC monolayers in the presence of anti-HA 3 HL60 cells competed with RBC for infected endothelial cells stained for cellular HA Ag and 4 anti- HA abolished the virus-induced adherence.
- Anatomy and Physiology