MONOCYTES AND POLYMORPHONUCLEAR NEUTROPHILS OF PATIENTS WITH STREPTOCOCCAL PHARYNGITIS EXPRESS INCREASED NUMBERS OF TYPE-I IGG FC-RECEPTORS

Studies using cultured cells have shown that gamma interferon (IFN-γ) induces the expression of FcγRI (the type I Fc receptor for IgF) on human polymorphonuclear neutrophils (PMN) and greatly increases the number of these receptors on human monocytes. Administration of rIFN-γ in vivo also causes enhanced FcγRI expression on these cell populations. Because streptococcal antigens are potent inducers of IFN-γ in vitro, we postulated that IFN-γ would be produced endogenously in vivo in patients with streptococcal infections. Such production of IFN-γ in vivo, even at low levels, might be expected to induce the expression of FcγRI on monocytes and neutrophils. To evaluate this possibility, we used monoclonal antibody 32 (mAb 32), which is specific for FcγRI, to quantitate the expression of this receptor on human peripheral blood cells. We measured the binding of mAb 32 to monocytes and PMNs isolated from healthy donors and from patients with group A β-hemolytic streptococcal (GABHS) pharyngitis. PMNs from healthy donors (n = 12) had 700 ± 600 (mean ±SD) mAb 32 binding sites. Patients with pharyngitis and negative throat culture for GABHS (n = 11) had 2,100 ± 1,600 sites on their PMNs. In contrast, the PMNs from patients with documented GABHS pharyngitis (n = 12) had 11,600 ± 7,500 mAb 32 binding sites on their surface. There was a similar change in the expression of FcγRI on monocytes, with control monocytes having a mean of 19,900 ± 3,200 mAb 32 binding sites per cell and the GABHS-positive monocytes having 47,500 ± 21,400 sites. The GABHS-negative throat culture group had a slightly elevated number of FcγRI with a mean of 28,200 ± 8,400 sites. 10 patients with documented urinary tract infections and three patients with uncomplicated pyelonephritis had no elevation in FcγRI expression. These studies demonstrate that a localized group A streptococcal infection can cause systemic activation of the entire circulating pool of phagocytes, and suggest that a similar level of activation is uncommon in localized gram-negative infections of the urinary tract.