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E-selectin-dependent neutrophil adhesion to Rickettsia rickettsii- infected
endothelial cells
LA Sporn, SO Lawrence, DJ Silverman and VJ Marder
Department of Medicine, University of Rochester School of Medicine and
Dentistry, NY 14642.
Increased neutrophil or HL60 cell adhesion to Rickettsia rickettsii-
infected endothelial cells (ECs) was observed at 6 to 8 hours after the
initiation of infection, diminishing by 24 hours. Similar increases were
observed using formaldehyde-fixed neutrophils. Cellular association and
likely the intracellular presence of rickettsiae was required for enhanced
neutrophil adhesion, because culture medium conditioned by infected cells
or rickettsiae rendered noninfective by pretreatment with tetracycline were
ineffective at inducing neutrophil adhesion. Increases in neutrophil
adhesion caused by infection were blocked by pretreatment of ECs with
cycloheximide, suggesting the involvement of new protein synthesis in the
cells' response. Flow cytometric analysis of infected cells showed
increases in cell surface expression of E-selectin compared with uninfected
control cells. Furthermore, incubation of 6- to 8-hour infected cells with
a blocking monoclonal antibody against E-selectin (BB11) inhibited
neutrophil adhesion an average of 61%. These results suggest the
involvement of E- selectin in neutrophil adhesion to infected ECs occurring
early in the course of the infection process. EC-initiated recruitment of
neutrophil adhesion during rickettsiae infection could contribute to the
pathologic changes associated with Rocky Mountain Spotted Fever.
Volume 81,
Issue 9,
pp. 2406-2412,
05/01/1993
Copyright © 1993 by The American Society of Hematology
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