Enhanced expression of Fc alpha receptor I on blood phagocytes of patientswith gram-negative bacteremia is associated with tyrosine phosphorylation of the FcR-gamma subunit

Sepsis caused by gram-negative bacteria is a common finding having high inc idence and mortality. Fc alpha RI (CD89), a receptor for immunoglobulin A ( IgA), has been shown to mediate bacterial phagocytosis, which might play a role in the pathogenesis of sepsis. In this study the expression and functi on of Fc alpha RI were analyzed on blood monocytes and neutrophils of patie nts with bacteremia. We found a marked increased in expression of the alpha - and gamma -subunits of the Fc alpha RI on both types of cells in patients with gram-negative bacteremia, but not in patients with gram-positive bact eremia. This increase was independent of serum IgA levels. Fc alpha RI M-r was lower on cells from gram-negative patients than on cells from controls (50-65 kDa versus 55-75 kDa), despite a similar 32-kDa backbone, indicating altered glycosylation. Increased levels of Fc alpha RI on blood phagocytes correlated with enhanced serum IL-6 levels, but not with IFN-gamma or TNF- alpha. FcR-gamma chain associated with Fc alpha RI was phosphorylated in pa tients neutrophils, indicating functional engagement of this receptor durin g gram-negative sepsis. Increased expression and activation of Fc alpha RI- gamma2 complexes following gram-negative infections suggests its involvemen t in host defense against bacteria.