FEBRILE INFECTION CHANGES THE EXPRESSION OF IGG FC-RECEPTORS AND COMPLEMENT RECEPTORS IN HUMAN NEUTROPHILS IN-VIVO

Citation
L. Leino et al., FEBRILE INFECTION CHANGES THE EXPRESSION OF IGG FC-RECEPTORS AND COMPLEMENT RECEPTORS IN HUMAN NEUTROPHILS IN-VIVO, Clinical and experimental immunology, 107(1), 1997, pp. 37-43
Citations number
36
Categorie Soggetti
Immunology
ISSN journal
00099104
Volume
107
Issue
1
Year of publication
1997
Pages
37 - 43
Database
ISI
SICI code
0009-9104(1997)107:1<37:FICTEO>2.0.ZU;2-H
Abstract
We have examined the expression of the Ige Fc receptors (FcRI, FcRII, FcRIII) and complement receptors (CR1, CR3) in neutrophils from 42 pat ients with febrile bacterial infection, 20 patients with febrile viral infection and 69 non-febrile healthy individuals. Using receptor-spec ific MoAbs and immunofluorescence flow cytometry the relative fluoresc ence intensity (as a measure of receptor number) and the proportion of receptor-positive cells were determined in peripheral blood neutrophi ls exposed to minimal processing, consisting only of erythrolysis. Bot h the percentage of FcRI-positive neutrophils and FcRI number per neut rophil were significantly (P < 0.001 and P < 0.0001) increased in bact erial infected patients compared with controls, whereas in viral infec ted patients only the FcRI percentage was markedly elevated (P < 0.05) . In addition, both FcRII and CR1 levels were significantly higher in the bacterial infection group than in the viral infection and control groups (bacterial versus control P < 0.001, bacterial versus viral P < 0.0001). No changes in expression of FcRIII or CR3 were found in the patient groups. The kinetic analysis of receptor expression in bacteri al infection patients revealed a shift in the percentage of FcRI-beari ng neutrophils towards normal values already on day 2 after the first analysis. On the other hand, the levels of FcRI, FcRII and CRI remaine d clearly elevated in these patients during 1 week's follow-up period. We conclude that febrile infection may cause systemic activation of t he entire pool of circulating neutrophils, resulting in alterations in cell surface receptor expression, some of which are characteristic of the nature of the infectious agent.