Studies on phagocytosis in patients with acute bacterial infections.

Abstract

Polymorphonuclear leukocytes (PMN) and monocytes from 20 patients with acute bacterial infections were examined for phagocytic function. PMN of patients expressed markedly enhanced phagocytosis as measured by the ingestion of erythrocyte (E)IgG and IgG/C3b-coated E. Phagocytosis of E coated with C3b alone was not seen, while low levels of ingestion of iC3b-E by patients' PMNs was noted. Monocytes from patients and controls expressed similar phagocytic activity in a fixed endpoint assay; however, the kinetics of phagocytosis by patients' monocytes was strikingly faster. Superoxide anion (02) and myeloperoxidase activities were similar to controls in PMN of four patients studied on day 1 of admission.PMN from two of three patients studied longitudinally showed an initial elevation in EIgG phagocytosis, which fell to normal levels by day 4, concomitantly with increased 0°gener-ation and clinical improvement. Phagocytosis remained elevated in the third patient who did not clear his septicemia.

Antigen targeting to myeloid-specific human Fc gamma RI/CD64 triggers enhanced antibody responses in transgenic mice.

“…PMN hFc␥RI was also up-regulated in mice with inflammatory lesions (Fig. 3 C), exactly as is observed in patients with bacterial infections (30). These results confirm that the human receptor is under strict control of endogenous mouse cytokines.…”

Genome-Wide Sequencing of Cellular microRNAs Identifies a Combinatorial Expression Signature Diagnostic of Sepsis

“…Neutrophil CD64 expression was first reported to be increased from patients with acute bacterial infection compared with healthy controls over 20 years ago [27]. A recent meta-analysis of 14 publications summarized that the average sensitivity and specificity of neutrophil CD64 was 79% and 91% respectively [28], which was reproduced in our study setting.…”

Leukocyte adhesion-deficient neutrophils fail to amplify phagocytic function in response to stimulation. Evidence for CD11b/CD18-dependent and -independent mechanisms of phagocytosis.

“…Evidence for exposure of both LAD and CGD PMN to inflammatory signals in vivo was given by the variable presence of FcRI on these patients' PMN. Normal resting PMN express minimal amounts ofFcRI, but its expression can be induced in vitro by exposure ofPMN to interferon-y (8) and it can be detected on the surface ofPMN isolated from patients with infectious diseases (25). CGD PMN (Fig.…”