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PubMed1987

Effect of human interferon on different functions of human neutrophils and eosinophils.

The capacity of neutrophils treated with interferon to release peroxidase or superoxide anion was increased when the cells were stimulated with opsonized zymosan, while it was decreased in eosinophils. The effect of treatment with interferon was thought to be mediated by a change in expression of C3b receptors on the neutrophils or eosinophils. The production of a slow-reacting substance of anaphylaxis by eosinophils stimulated with opsonized zymosan or human IgG-coupled Sepharose 4B beads was markedly enhanced after incubation with interferon. Therefore it is suggested that interferon may play a role in the worsening of the condition in patients with bronchial asthma.

Asthma↗
PubMed1987

Effect of polymeric IgG on human monocyte functions.

Fc and iC3b receptors are involved in various biological functions of phagocytic cells, such as immune adherence and phagocytosis of opsonized particles, degranulation and superoxide generation. In the present study we examined the expression of specific receptors for the Fc portion of IgG (FcR) and for iC3b (CR3), a cleavage product of the third complement component, on human monocytes following in vitro treatment with polymeric and monomeric IgG. Interaction of polymeric IgG (fluid phase) with the monocyte membrane led to a concomitant modulation of both Fc and iC3b receptors. Monomeric IgG, however, down modulated Fc receptor expression only if surface bound. Under these conditions, no concomitant modulation of the iC3b receptor could be observed. The down modulation of Fc and iC3b receptors induced by fluid-phase IgG polymers was also accompanied by a decrease in monocyte functions as expressed by reduced Fc receptor-mediated phagocytosis, decreased release of oxygen metabolites following stimulation by aggregated IgG and opsonized zymosan, as well as in impaired killing of bacteria. These data suggest that a down modulation of Fc and iC3b receptors might have important implications for host defense mechanisms, since interaction with these receptors is required for the proper elimination of many pathogens.

Blood Bactericidal Activity↗
PubMed1989

Effects of clindamycin and cefuroxime on leukocyte membrane receptors and function.

Normal human granulocytes and lymphocytes were preincubated in 0.5, 5, or 50 mg/l of clindamycin, and 5, 50, or 500 mg/l of cefuroxime. Incubation with clindamycin caused an increase in the proportion of granulocytes bearing receptors for the Fc portion of IgG (Fc gamma-R) and C3b (C3b-R). Random migration in capillary tubes was significantly decreased, but phagocytosis as measured by chemiluminescence was only slightly decreased. The proportion of lymphocytes bearing Fc gamma-R was decreased, while there was no effect on lymphocyte C3b-R percentage, nor on the proportion of granulocytes or lymphocytes bearing sheep erythrocyte (E) receptors. Preincubation of granulocytes in cefuroxime was not associated with changes in the proportion of receptor-bearing cells, except for a slight increase in Fc gamma-R-bearing lymphocytes at the lowest concentration tested. Tube migration was not affected but chemiluminescence was significantly decreased. Preincubation with clindamycin, although increasing the proportion of cells bearing phagocytosis-associated receptors, is thus not associated with an increased phagocytic ability, while cefuroxime incubation caused a decrease in chemiluminescence despite normal levels of receptor-positive cells.

Antigens, Differentiation↗
PubMed1995

Neutrophils from preterm neonates and adults show similar cell surface receptor expression: analysis using a whole blood assay.

Previous work has shown that Fc gamma RIII expression in isolated neonate neutrophils is defective. We have re-examined this phenomenon in view of the facts that (1) the receptor is present on mobilisable subcellular stores and (2) commonly used isolation procedures can affect receptor expression in suspensions of isolated neutrophils. Receptor expression was measured by fluorescence-activated cell sorter analysis of neutrophils in unfractionated whole blood. Examination of receptor expression in preterm, term and adult neutrophils indicated small but significantly decreased expression of CR1 and CR3 in preterm neutrophils compared with term neutrophils (p < 0.01). A small decrease in expression was found for Fc gamma RI and Fc gamma RIII (p < 0.05). No significant difference in expression of Fc gamma RII was observed in all groups analysed. These data suggest that isolated preterm neonate neutrophils have greatly decreased expression of Fc gamma RIII because of impaired composition or mobilisation of the subcellular stores of this receptor and/or increased lability of the surface receptor which leads to its shedding during purification.

Adult↗
PubMed1987

Specificity of membrane complement receptor type three (CR3) for beta-glucans.

The binding of the iC3b receptor (CR3) to unopsonized zymosan was shown to result from CR3 attachment to cell wall beta-glucans. A specificity of neutrophil responses for beta-glucan was first suggested by a comparison of yeast (Saccharomyces cerevisiae) cell wall components for stimulation of a neutrophil superoxide burst. Neutrophils responded poorly to heat-killed yeast, but gave increasingly better responses to cell wall polysaccharides devoid of proteins (zymosan) and nearly pure beta-glucan particles derived from zymosan. Zymosan triggered a burst that was 29% as great as that stimulated by phorbol myristate acetate (PMA), and beta-glucan particles stimulated a burst that was 72% as great as that produced by PMA. Phagocytic responses to yeast were also inhibited by soluble glucans but not by soluble mannans. Three types of experiments demonstrated a role for CR3 in these responses. First, neutrophil ingestion of either yeast or yeast-derived beta-glucan particles was blocked by monoclonal anti-CR3, fluid-phase iC3b, or soluble beta-glucan from barley. Monocyte ingestion of beta-glucan particles was also blocked by anti-CR3, but not by anti-CR1 or anti-C3. Second, the neutrophil superoxide burst response to either zymosan or beta-glucan particles was blocked by anti-CR3 or fluid-phase iC3b, and was completely absent with neutrophils from 3 patients with an inherited deficiency of CR3. Third, CR3 was isolated from solubilized neutrophils by affinity chromatography on beta-glucan-Sepharose.

Glucans↗
PubMed1989

Deficient intracellular killing of bacteria by murine alveolar macrophages.

Microbiologic methods were used to assess the in vitro phagocytosis and intracellular killing of various species of bacteria by freshly isolated murine peritoneal and alveolar macrophages. Peritoneal macrophages showed effective phagocytosis of opsonized Streptococcus pneumoniae, Streptococcus pyogenes, Pseudomonas aeruginosa, Staphylococcus epidermidis, and Listeria monocytogenes, and moderate ingestion of Staphylococcus aureus and Escherichia coli. Alveolar macrophages were poor in phagocytosing opsonized S. pyogenes, S. aureus, and E. coli; ingestion of S. pneumoniae, P. aeruginosa, and S. epidermidis was moderate. Peritoneal macrophages killed 40 to 80% of these bacteria intracellularly, but alveolar macrophages showed almost no intracellular killing of bacteria. To find out whether there is a correlation between the poor bactericidal activity of alveolar macrophages and the oxygen-dependent microbicidal mechanisms of these cells, we determined the uptake of oxygen and the release of superoxide anion and hydrogen peroxide by macrophages at rest and after stimulation with phorbol myristate acetate (PMA) or opsonized S. aureus. Upon exposure to these stimuli, peritoneal macrophages, but not alveolar macrophages, showed an increased uptake of oxygen and release of superoxide anion and hydrogen peroxide. Because alveolar macrophages contain surface active material (SAM), we investigated the phagocytosis and intracellular killing of bacteria and the release of hydrogen peroxide by peritoneal macrophages pretreated with SAM. The results showed reduced phagocytosis and impaired intracellular killing of S. epidermidis by these macrophages. The release of hydrogen peroxide by SAM-pretreated peritoneal macrophages upon stimulation with PMA or opsonized S. aureus was equal to that of the control peritoneal macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Ontogeny of Fc receptors and complement receptor (CR3) during human myeloid differentiation.

Two different Fc receptors for IgG (Fc gamma R) have been identified on human leukocytes: a high avidity receptor (Fc gamma Rhi) present on monocytes but not on neutrophils, and a low avidity receptor (Fc gamma Rlo) present on neutrophils but not on monocytes. Fc gamma Rlo can be inhibited and the receptor precipitated by monoclonal antibody 3G8. We have used this monoclonal antibody to study the course of Fc gamma Rlo appearance on bone marrow cells, leukocytes of patients with chronic myelogenous leukemia (CML), and HL-60 and U937 cells induced to differentiate with agents such as dimethyl sulfoxide (DMSO), retinoic acid, phorbol myristate acetate, and lymphokine. We report that Fc gamma Rlo is a late differentiation antigen, first expressed at the metamyelocyte stage. Since precursors to metamyelocytes bear Fc gamma R, and the promyelocyte line HL-60 bears Fc gamma Rhi, there must be a progressive loss of Fc gamma Rhi during myeloid differentiation and the reciprocal expression of Fc gamma Rlo. Results of immunoprecipitation and polyacrylamide gel analysis of the proteins are consistent with these results. We have also studied the receptor for the C3bi complement component (CR3), which is blocked and immunoprecipitated by monoclonal antibody OKM10. During DMSO-driven differentiation of HL-60 cells, we find that CR3 is induced on all cells, whereas Fc gamma Rlo is induced on only 24% of cells, suggesting that CR3 appears earlier during differentiation than Fc gamma Rlo does.

Antibodies, Monoclonal↗
PubMed1984

Human neutrophils increase expression of C3bi as well as C3b receptors upon activation.

We used monoclonal antibodies and flow cytometry to study the expression of the receptors for the complement fragments C3bi (CR3) and C3b (CR1) on human polymorphonuclear neutrophil leukocytes (PMN). Expression of both receptors was minimal on cells stained in anticoagulated whole blood incubated at 0 degree or 37 degrees C. PMN isolated with Percoll density gradients and held at 0 degree C also had only minimal expression of both receptors. With the isolated cells, however, a spontaneous increase in expression of both receptors occurred upon warming to 37 degrees C. This did not represent complete expression of either receptor since additional increments in surface expression could be induced upon stimulation with N-formyl-methionyl-leucyl-phenylalanine or Raji cell supernatant. The increases in complement receptor (CR) expression appeared to be specific since there were no changes in expression of the Fc gamma receptor or beta-2-microglobulin under any of these conditions. The increased CR expression seems to involve translocation from an intracellular pool since it is complete within minutes and is not blocked by puromycin or cycloheximide. These results demonstrate that both CR3 and CR1 expression increase rapidly upon activation of PMN and that isolated cells can be used to study this phenomenon, which may be a critical part of neutrophil function in vivo.

Antibodies, Monoclonal↗
PubMed1986

Comparison of intravenous gamma globulin and a monoclonal anti-Fc receptor antibody as inhibitors of immune clearance in vivo in mice.

Fc-receptor-mediated clearance and nonspecific phagocytic clearance were assessed after the infusion of monomeric human IgG, heat-aggregated human IgG, and a monoclonal anti-mouse macrophage FcII receptor antibody (2.4G2) into normal mice. Each agent blocked Fc-receptor function in vivo, but 2.4G2 was much more potent per microgram than the other agents. Monomeric IgG in blocking doses did not affect other aspects of immune function. In contrast, aggregated IgG, and to a lesser extent, 2.4G2 reduced serum complement levels. In addition, these agents also caused moderate reductions in nonspecific phagocytic function. Monoclonal anti-mouse macrophage C3bi receptor antibody (Mac-1), another monoclonal antibody which binds to macrophage CR3 receptors without interfering with Fc-receptor function, also reduced serum complement and inhibited nonspecific phagocytic function. Complement depletion alone (produced by infusion of cobra venom factor) could not account for the observed changes in Fc receptor or nonspecific phagocytic function. We conclude that both monomeric IgG and anti-Fc-receptor antibodies can markedly inhibit Fc-receptor function in vivo; however, the pattern of physiologic changes produced by these agents differs.

Animals↗
PubMed1988

Mechanism of inhibition of immunoglobulin G-mediated phagocytosis by monoclonal antibodies that recognize the Mac-1 antigen.

We have investigated the effects of the monoclonal antibodies against the cell surface molecule Mac-1 on C3bi-mediated rosetting and IgG-mediated rosetting and phagocytosis by human peripheral blood monocytes. Highly purified M1/70 F(ab')2, used in the fluid phase, inhibited both monocyte functions. Half-maximal C3bi rosette inhibition occurred at a concentration of 2 nM F(ab')2 M1/70. An equivalent decrease in IgG-mediated rosetting required 10 nM M1/70 F(ab')2, and 50% inhibition of IgG-mediated phagocytosis required 7 nM antibody. Mo-1 F(ab')2 inhibited EC3bi binding with an ID50 of 0.3 nM, whereas 50% decrease in IgG-mediated rosetting required 70 nM of this antibody. OKM1 did not inhibit rosettes of sheep erythrocytes opsonized with IgG antibody (EA) at all. F(ab')2 M1/70 did not affect the binding of monomeric human IgG to monocytes, but did substantially decrease the binding of IgG aggregates. Half-maximal inhibition of aggregated IgG binding at 0 degrees C occurred at 8 nM F(ab')2 M1/70, very close to the concentration that caused equivalent inhibition of IgG-mediated phagocytosis. Aggregated IgG inhibited the binding of radiolabeled M1/70 to monocytes by approximately 40%, suggesting that some, but not all Mac-1 molecules were associated with IgG receptors under these conditions. When cells were allowed to adhere to surfaces coated with M1/70 or Mo-1 F(ab')2, C3bi-mediated rosetting was inhibited, but IgG mediated-phagocytosis was unaffected. Moreover, the dose response of inhibition of phagocytosis by fluid-phase F(ab')2, of anti-Mac-1 monoclonals was similar on monocytes adherent to albumin-coated and antibody-coated surfaces. Kinetic experiments showed that even prolonged incubation of monocytes on M1/70 coated surfaces did not lead to inhibition of EA binding nor did these incubations alter the dose response for inhibition of EA binding by fluid-phase M1/70 F(ab')2. This suggested that not all molecules recognized by M1/70 are freely mobile in the plasma membrane. Indeed, only approximately 60% of 125I-M1/70-biding sites were lost even after 4 h when monocytes were adherent to M1/70-coated surfaces. We conclude that some anti-Mac-1 antibodies can inhibit EA binding because of their epitope specificity, independent of any direct interaction with monocyte Fc receptors. This interference with IgG-Fc receptor-mediated binding and ingestion apparently occurs because of antibody binding to a subpopulation of Mac-1 molecules which are associated with IgG Fc receptors and remain on the apical membrane of monocytes adherent to anti-Mac-1-coated surfaces. We suggest that there may be two functionally distinct molecules on human monocytes recognized by M1/70 and Mo-1 that can be distinguished by their mobility in the plane of the monocyte membrane. The more mobile form of Mac-1 is involved in C3bi rosettes, and does not affect IgG-mediated phagocytosis. The other antigen recognized by M1/70 does not diffuse within the plane of the membrane; ligation of the latter molecule by antibody is associated with inhibition of IgG-mediated phagocytosis.

Antibodies, Monoclonal↗
PubMed1988

Lymphocytes expressing type 3 complement receptors proliferate in response to interleukin 2 and are the precursors of lymphokine-activated killer cells.

In the absence of antigenic or mitogenic stimulation, certain peripheral blood lymphocytes exhibit proliferative and lymphokine-activated killer (LAK) cell activities when cultured with recombinant IL-2. Both activities were found to be an exclusive property of lymphocytes expressing type 3 complement receptors (CR3) identified by anti-CD11 monoclonal antibodies. CD11+ lymphocytes were then fractionated into three subsets by two-color flow cytometry. These included CD16+ cells, which display distinctive Fc receptors for IgG (CD16). Using anti-CD5, the CD11+ CD16- lymphocytes were separated into non-T cell and T cell subsets. The two non-T cell subsets (CD11+ CD16+ and CD11+ CD16- CD5-), but not the T cell subset (CD11+ CD16- CD5+), could proliferate in response to IL-2. Both CD11+ non-T cell subsets, but not the CD11+ T cell subset, had the capacity to mediate natural killer cell activity. However, all three CD11+ lymphocyte subsets were capable of generating LAK activity. These findings are consistent with the concept that two signals are required to stimulate T cells to proliferate. However, at least a small subset of blood T cells can be activated by IL-2 to become LAK cells.

Antigens, Differentiation↗
PubMed1989

Characterization and cytoskeletal association of a major cell surface glycoprotein, GP 140, in human neutrophils.

The binding of specific ligands to neutrophil cell surface receptors and the association of these receptors with the cytoskeleton may represent an essential step in activation. To identify surface proteins that are linked to the cytoskeleton during activation, neutrophil 125I-surface labeled plasma membranes were extracted with Triton X-100, and the soluble and insoluble (cytoskeleton) fractions analyzed by SDS-PAGE and autoradiography. The major cell surface proteins recruited to the cytoskeleton after activation with Con A, FMLP, zymosan-activated serum, or immune complexes possessed a relative molecular mass in the range of 80 to 13 kD. In addition to these proteins, WGA stimulates the recruitment of a 140-kD protein (GP 140) to the cytoskeletal fraction. That GP 140 is a WGA-binding protein was verified by Western blotting and WGA-Sepharose affinity chromatography. The Coomassie blue staining pattern of the WGA cytoskeletal fraction revealed major protein bands at apparent molecular weights of greater than 200 (approximately 250, 240, 235), 200, 115, 82/78 (a doublet), 56, 43, 36, and 18 kD. Labeling cells with 32PO4 before WGA treatment indicated that the cytoskeletal proteins with molecular weights of 115, 82/78, and 72 kD, and a 40-kD detergent soluble protein, are phosphorylated during activation. The 78 kD cytoskeletal phosphoprotein co-migrates with the lower subunit of erythrocyte (RBC) band 4.1 and shows strong cross-reactivity with RBC anti-band 4.1 antibody. Phosphorylation of cytoskeletal proteins like 4.1 may be involved in the regulation of interactions between GP 140 and the actin-containing cytoskeleton. Unlike the C3bi receptor, GP 140 is a major surface component of unactivated PMNs, has no stoichiometrically related 95-kD subunit, and has two isoforms with pIs in the range of 6.4 to 6.6. Under conditions that result in an increased expression of the C3bi receptor (such as treatment with the Ca2+ ionophore A23187), the amount of GP 140 on the PMN cell surface appears to be significantly reduced. The interaction of GP 140 with the cytoskeleton during activation suggests that GP 140 may play an important role in neutrophil functional responses.

Actins↗
PubMed1989

Receptor-mediated phagocytosis in human neutrophils is associated with increased formation of inositol phosphates and diacylglycerol. Elevation in cytosolic free calcium and formation of inositol phosphates can be dissociated from accumulation of diacylglycerol.

Phagocytosis of C3bi- or IgG-opsonized yeast particles in human neutrophils was found to be associated with an increased formation of inositol phosphates and diacylglycerol. Pertussis toxin only marginally affected phagocytosis of IgG- and C3bi-opsonized particles and the associated formation of second messengers. Forskolin, which induced a threefold rise of cellular cAMP, however, markedly inhibited both C3bi- and IgG-mediated phagocytosis as well as the particle-induced formation of inositol phosphates and diacylglycerol. These observations are in contrast to what was found to occur with chemotactic factors and indicate that chemotactic and phagocytic signaling can be regulated independently in human neutrophils. Since C3bi-mediated phagocytosis has been shown to occur at vanishingly low cytosolic free calcium levels, calcium-depleted cells were used to study the importance of the inositol cycle for the engulfment of C3bi-opsonized particles. Despite a total lack of receptor-induced formation of inositol phosphates, a significantly increased accumulation of diacylglycerol accompanied the ingestion of C3bi-opsonized particles. These data show that the engulfment of C3bi-opsonized particles can occur independently of both a calcium transient and an increased inositol phosphate production. However, the observed accumulation of diacylglycerol, not derived from phosphoinositides, suggests that this second messenger play a role in the control of the engulfment process.

Antigens, Differentiation↗
PubMed2002

Manipulation of lymphoid microenvironments in nonhuman primates by an inhibitor of the lymphotoxin pathway.

Reticular networks in lymphoid organs play critical roles in the organization of local microenvironments. A number of these elements are maintained by continual signaling through the lymphotoxin system. Evaluation of the lymphotoxin (LT) pathway in primates using a fusion protein decoy provides a unique opportunity to assess modulation of splenic microenvironments in a species with considerably greater background immunological activity compared with rodents. Within the germinal center microenvironment, treatment resulted in a collapse of follicular dendritic cell (FDC) networks and in the disappearance of a ringlike network of immune complex-carrying cells, although some other attributes of the germinal center appeared to be unaltered. Treatment also resulted in changes in the splenic marginal zone, a microenvironment where the architecture is notably different from that of the rodent. Cessation of treatment and recovery allowed us to monitor reemergence of these cell types and revealed that FDCs rely on LT-dependent signals to recompact into appropriately positioned tight networks. Despite the loss of FDC networks, the primary Ab response to keyhole limpet hemocyanin was unaltered over a 20-day period. Manipulation of these microenvironments may represent a novel approach to modulating immune function in human disease.

Animals↗
PubMed1989

Development of surface membrane characteristics of "premedullary" macrophages in organ cultures of embryonic rat and hamster lungs.

A replicating population of non-monocyte-derived free cells appears in organ-cultured embryonic rat lungs, indistinguishable from alveolar macrophages by classical criteria such as ultrastructure, lysosomal enzyme cytochemistry, and phagocytic behavior. We demonstrate similar events in cultured embryonic hamster lungs and development of macrophage-associated properties on the plasmalemma of these cells in both species. Immunoperoxidase localizations were obtained using monoclonal antibodies against alveolar macrophage antigen (HAM1) in hamsters, and rat macrophage antigen (ED1) and leukocyte-common antigen (OX1) in rats. Fc and C3b receptors were identified in both species by immune rosetting. HAM1 staining, perinuclear in rare cells at explantation, gains definitive surface localization 3-4 days later as cells prepare to emerge through the pleura. ED1 and OX1 cytoplasmic staining first occurs after 24 hr, increases as macrophages multiply and congregate beneath the pleura, and translocates to the plasmalemma of emerged cells. Some glass-adherent cells from lung explants have Fc receptors. The proportion rises sharply for 24 hr and equals fully emerged cells (90-95%) by days 3-4. At first phagocytosis is slow to follow Fc receptor binding, but ingestion time decreases to 3-10 min as macrophages mature. A minority of emerged macrophages bind complement-opsonized erythrocytes, which are rarely taken up. These properties are shared by alveolar macrophages of adults.

Animals↗
PubMed2002

Complement-mediated clearance of erythrocytes: mechanism and delineation of the regulatory roles of Crry and DAF. Decay-accelerating factor.

The role of complement in the pathogenesis of autoimmune hemolytic anemia (AIHA) has been controversial and may depend on a number of factors, including the affinity and isotype of the pathogenic antibodies involved. We have recently shown that mouse erythrocytes deficient in the membrane C3 regulatory protein, complement receptor 1-related gene/protein y (Crry), but not decay-accelerating factor (DAF), were spontaneously eliminated in vivo by complement. Here, by generating a mouse deficient in both DAF and Crry, we further delineated the roles of Crry and DAF in regulating alternative and classical pathway C3 activation. By using immunoglobulin-, Fcgamma receptor (FcgammaR)-, C3-, C4-, and C5-deficient mice, we also determined the mechanism by which membrane C3 regulator-deficient erythrocytes are cleared from the circulation. Finally, we evaluated the relative importance of the Fc receptor versus the complement pathway in disposing antibody-opsonized DAF/Crry-deficient erythrocytes. We conclude that (1) Crry plays a more dominant role than DAF in regulating the alternative pathway of complement, whereas DAF and Crry are equally effective in preventing antibody-induced runaway complement activation on mouse erythrocytes; (2) DAF/Crry-deficient erythrocytes are eliminated by the alternative pathway of complement via complement receptor-mediated erythrophagocytosis in the spleen; and (3) when opsonized with an immunoglobulin G2a (IgG2a) autoantibody, Crry/DAF-deficient erythrocytes are eliminated more rapidly by complement than by the Fc receptor pathway. These results shed new light on the relative activities of Crry and DAF and underscore the critical roles of membrane C3 regulators in preventing spontaneous and antibody-induced erythrocyte damage in vivo.

Agammaglobulinemia↗
PubMed1984

Characteristics and functional capacities of human cord blood granulocytes and monocytes.

Cord blood phagocytic cells were characterized with respect to cytochemical activities, Fc gamma and C3b receptors, and capacity to phagocytose and kill various species of bacteria. The percentages of peroxidase-positive granulocytes and monocytes from neonates and adults were comparable; the percentage of esterase-positive cord-blood monocytes was about two-thirds of that of adults' blood monocytes. The numbers of cord blood and adults' monocytes with Fc gamma and C3b receptors were similar. Phagocytic and intracellular killing capacities of cord blood granulocytes and monocytes were investigated for Staphylococcus aureus, Escherichia coli, Streptococcus pyogenes, and group B Streptococcus type III. The rates of phagocytosis and intracellular killing by granulocytes from newborns proved to be comparable to the corresponding values for granulocytes from adults. Cord blood monocytes phagocytosed E. coli, S. aureus, and S. pyogenes at a normal rate, and killed ingested E. coli and S. pyogenes intracellularly at the same rate as adults' monocytes did. However, S. aureus was killed at a much lower rate by cord blood monocytes than by monocytes from adults. Phagocytic activity for group B Streptococcus was impaired and killing of these bacteria by cord blood monocytes was virtually nil. The latter finding might partially explain the frequent streptococcal infections in newborns.

Adult↗
PubMed1990

Expression of the complement receptors CR1 and CR3 and the type III Fc gamma receptor on neutrophils from newborn infants and from fetuses with Rh disease.

Developmental defects in neutrophil function, including diminished expression of plasma membrane receptors, may play an important role in the susceptibility of the newborn infant to infection. We used monoclonal antibodies and flow cytometry to study the expression of complement receptor type one (CR1), complement receptor type three (CR3), and Fc gamma receptor type three (FcRIII) on neutrophils from six fetuses with Rh disease, 10 preterm infants, nine term infants, and nine adults. Expression of the complement receptors on unstimulated cells was similar for all groups, but significant differences in complement receptor expression were observed after stimulation with N-formyl-methionyl-leucyl-phenylalanine (FMLP). Fetal, preterm, and term infant neutrophils expressed less CR3 than FMLP-stimulated neutrophils of adults [61 +/- 2, 48 +/- 4, and 66 +/- 4% (mean +/- SEM) of the mean for adults, p less than 0.05]. FMLP-stimulated CR1 expression for these groups was 61 +/- 6, 73 +/- 6, and 91 +/- 9% of the adult mean (p less than 0.05, fetal versus term infant and adult). Expression of both CR3 and CR1 increased with postconceptional age in the infants (r2 = 0.49, p less than 0.001 for CR3; r2 = 0.23, p less than 0.05 for CR1). Neutrophils of the preterm and term infants expressed less FcRIII than adult neutrophils (68 +/- 10 and 77 +/- 7% of the adult mean, p less than 0.05, for FMLP-stimulated cells), whereas fetal neutrophil FcRIII expression did not differ from that of the adult.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, Differentiation↗