The effects of substance P on human eosinophil receptors and functions.
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Antibody-Dependent Cell Cytotoxicity↗
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Phagocytosis, peritoneal influx, and enzyme activities in peritoneal macrophages from germfree, conventional, and ex-germfree mice.
Peritoneal macrophages from germfree mice showed a higher basic activity of lysosomal enzymes than did macrophages from conventional mice, whereas oil-induced peritoneal influx, induction of lysosomal enzymes, and phagocytosis via the C3b receptor after endotoxin stimulation were reduced or absent. After germfree mice had been housed with conventional mice for 1 week, peritoneal influx and C3b receptor-mediated phagocytosis reached normal levels; after 4 weeks, enzyme activities also reached normal levels.
Acid Phosphatase↗
Extracellular stimulation by serum proteins required for maximal intracellular killing of microorganisms by mouse peritoneal macrophages.
Intracellular killing of catalase-positive Staphylococcus aureus by resident mouse peritoneal macrophages was very low in the absence of serum but maximal in the presence of fresh normal serum. A large proportion of catalase-negative Streptococcus pyogenes were killed in the absence of extracellular serum, and maximal killing was reached only when serum was present extracellularly. Further investigations revealed that stimulation of intracellular killing by extracellular serum is dependent on the interaction of immunoglobulin G and Fc receptors and of complement component C3b with C3b receptors in the macrophage membrane.
Animals↗
Roles of CR3 and mannose receptors in the attachment and ingestion of Leishmania donovani by human mononuclear phagocytes.
Leishmania donovani is an obligate intracellular parasite of mammalian macrophages. Two macrophage receptors, the mannose-fucose receptor (MFR) and the receptor for complement component C3bi, CR3, were examined for their roles in the attachment and ingestion of L. donovani by human monocyte-derived macrophages. Two monoclonal antibodies which bind to the human CR3, anti-Mo1 and anti-Mac-1, inhibited both attachment and ingestion of L. donovani promastigotes after preincubation with human monocyte-derived macrophages; attachment was inhibited by 40 and 62% by anti-Mo1 and anti-Mac-1, respectively, and ingestion was inhibited by 34 and 51% by anti-Mo1 and anti-Mac-1, respectively. The interaction between promastigotes and CR3 may not have involved the C3bi-binding site on CR3, however, because a monoclonal antibody which exhibits specificity for this site, OKM10, inhibited promastigote attachment by only 18%. In contrast, OKM1, which is believed to react with the alternate lectinlike binding site on CR3, inhibited ingestion by 65%. MFR activity was inhibited using the soluble MFR ligands, mannan and mannosylated bovine serum albumin, which also inhibited promastigote attachment by 40 and 37%, respectively. The simultaneous inhibition of both CR3 (by anti-Mac-1) and the MFR (by either mannan or mannosylated bovine serum albumin) resulted in a greater decrease in promastigote attachment than inhibition of either receptor alone. Additionally, the reduction of MFR activity by allowing macrophages to adhere to a mannan-coated surface followed by the addition of anti-CR3 antibodies resulted in an 81% inhibition of promastigote ingestion, a greater decrease than was obtained by manipulation of either receptor alone. The results suggest that the MFR and CR3 independently participate in the attachment and ingestion of L. donovani promastigotes by human macrophages.
Animals↗
Changes in complement and immunoglobulin G receptor expression on neutrophils associated with Porphyromonas gingivalis-induced inhibition of phagocytosis.
We examined the phagocytic capacity and receptor expression on neutrophils stimulated with Porphyromonas gingivalis soluble products. Stimulated neutrophils had decreased phagocytic capacities and altered expression of CR1, CR3, Fc gamma RII, and Fc gamma RIII. For cases in which TLCK (N-alpha-p-tosyl-L-lysine chloromethyl ketone) neutralized the effects of the stimuli, the P. gingivalis-derived factors causing the phenomena seem to be trypsin-like proteases.
Humans↗
Lipopolysaccharide-induced granule mobilization and priming of the neutrophil response to Helicobacter pylori peptide Hp(2-20), which activates formyl peptide receptor-like 1.
The cecropin-like bactericidal peptide Hp(2-20) from Helicobacter pylori induces activation of the NADPH oxidase in human neutrophils via formyl peptide receptor-like 1 (FPRL1) (J. Bylund, T. Christophe, F. Boulay, T. Nyström, A. Karlsson, and C. Dahlgren, Antimicrob. Agents Chemother. 45:1700-1704, 2001). Here we investigated the ability of bacterial lipopolysaccharide (LPS) to prime this response. Neutrophils treated with LPS for 30 min at 37 degrees C produced substantially more superoxide anion than control cells upon stimulation with Hp(2-20). Hence, LPS primed the cells for subsequent stimulation through FPRL1. To study the molecular background of this priming phenomenon, we measured the degrees of granule mobilization and concomitant receptor upregulation to the cell surface in LPS-treated cells. Exposure of complement receptors 1 and 3 as well as the formyl peptide receptor (FPR) was markedly increased after LPS treatment. Since approximately 60% of the gelatinase granules were mobilized while the specific granules were retained, we hypothesized that the gelatinase granules were potential stores of FPRL1. The presence of FPRL1 mainly in the gelatinase granules was confirmed by Western blotting of subcellular fractions of resting neutrophils. These results suggest that the mechanism behind the LPS-induced priming of FPRL1-mediated responses lies at the level of granule (receptor) mobilization.
Amino Acid Sequence↗
Functional defects of monocyte C3b receptor-mediated phagocytosis in rheumatoid arthritis (RA): evidence for an association with the appearance of a circulating population of non-specific esterase-negative mononuclear phagocytes.
We have previously described a selective defect of monocyte C3b receptor-mediated phagocytosis in patients with rheumatoid cutaneous vasculitis. We have studied a further 15 rheumatoid arthritis patients with other associated diseases and complications and have identified 4 further patients with a similar defect. Serological and cytochemical studies suggest that the defect in phagocytosis is due to the appearance of increased numbers of large nonspecific esterase-negative mononuclear phagocytes with defective C3b receptor phagocytic function rather than to receptor blockade by immune complexes.
Adult↗
Receptor expression in synovial fluid neutrophils from patients with rheumatoid arthritis.
OBJECTIVES: The aim of this study was to determine if neutrophils isolated from the blood and synovial fluid of patients with rheumatoid arthritis had patterns of receptor expression resembling those of blood neutrophils from controls which had been activated and primed in vitro. METHODS: Fluorescence activated cell sorting was used to measure receptor expression in paired blood and synovial fluid neutrophils from patients and in control neutrophils exposed to phorbol myristate acetate and granulocyte-macrophage colony stimulating factor. RESULTS: There was no significant difference in the patterns of receptor expression in blood neutrophils from patients and healthy controls, but neutrophils in the synovial fluid had been primed and activated within the joint. About 50% of rheumatoid synovial fluid neutrophil samples expressed Fc gamma RI, a high affinity receptor for monomeric IgG, which is only expressed in neutrophils exposed to cytokines. CONCLUSIONS: Synovial fluid neutrophils are activated and primed within the inflamed joint and hence their ability to respond to activating factors such as immune complexes will be modulated. As the expression of Fc gamma RI requires active biosynthesis, this work indicates that selective gene activation occurs when neutrophils are recruited into rheumatoid joints.
Antigens, CD↗
Mononuclear cell complement receptor blockade in primary biliary cirrhosis.
Peripheral blood monocyte and lymphocyte receptors for Fc and C3b fragments were examined in vitro in patients with primary biliary cirrhosis and other chronic liver diseases using sheep red blood cells coated with anti-SRBC IgG1 (to detect Fc receptors) and with anti-SRBC IgM and complement (to detect C3b receptors). The number of C3b receptors detected on 100 monocytes was significantly lower in patients with primary biliary cirrhosis (23.0 +/- 12.0, mean +/- 1 SD) compared with normal controls (57.4 +/- 16.9) and other chronic liver disease (HBsAg negative chronic active hepatitis 62.0 +/- 17.0, alcoholic cirrhosis 50.9 +/- 4.0), while the number of Fc receptors detected on 100 monocytes was not significantly different in all the groups (primary biliary cirrhosis 72.8 +/- 28.6, chronic active hepatitis 74.7 +/- 14.0, alcoholic cirrhosis 58.0 +/- 13.5 and normal controls 69.6 +/- 19.9). When mononuclear cells isolated from normal individuals were pre-incubated with serum from patients with primary biliary cirrhosis before testing their receptor function there was a significant reduction in the number of C3b receptors detected per 100 monocytes (27.6 +/- 10.8) compared with pre-incubation with normal serum (72.0 +/- 18.0). This reduction in C3b-receptor function was again observed when the serum used for pre-incubation was depleted of circulating immune complexes; but when complement was further depleted from these sera, the number of C3b-receptors detected after pre-incubation was similar to normal values (64.0 +/- 11.8). Lymphocyte receptors showed a similar pattern of results. This implies a specific C3b receptor blockade on monocytes and lymphocytes from patients with primary biliary cirrhosis which appears to be because of blocking by serum factor(s) including complement fragments.
Adult↗
Membrane Fc-IgG and C3b receptors on myeloid leukaemia cells: a comparison with cytoplasmic acid naphthyl acetate esterase cytochemistry.
Membrane receptors for IgG and C3b were examined on blast cells from 57 cases of acute myeloid leukaemia. These acute leukaemias were classified as myeloblastic, myelomonocytic or monocytic following morphological, cytochemical, and immunological investigations. The membrane receptors of leukaemic blast cells appear to be directly related to the degree of monocytic differentiation with the lowest receptor activities found in acute myeloblastic leukaemia. A comparison was also made between receptor and cytoplasmic acid naphthyl acetate esterase (ANAE) activities in 29 morphologically and immunologically-defined myelomonocytic and monocytic leukaemias. This study revealed that the receptor-positive "monocytic component" in a significant proportion of cases showed unexpectedly weak or negative ANAE reactions suggesting a more cautious approach to the interpretation of ANAE cytochemistry in acute leukaemias. The normal development of cytoplasmic ANAE and membrane receptors is also discussed and compared with their abnormal patterns of expression associated with leukaemic transformation.
Carboxylic Ester Hydrolases↗
Mononuclear leucocyte function tests in the assessment of the biocompatibility of peritoneal dialysis fluids.
BACKGROUND: Previous studies showed that the currently used dextrose based peritoneal dialysis fluids impair several leucocyte functions. AIMS: To determine which in vitro mononuclear leucocyte (monocyte) function tests most clearly reflect the biocompatibility of peritoneal dialysis fluid. METHODS: Monocytes were tested for phagocytic capacity, bactericidal activity, Fc and C3 receptor expression, and chemiluminescence response, and by analysis of the release of interleukin 8 (IL-8) and tumour necrosis factor alpha (TNF alpha) in the presence of test fluids. Cytokine release was studied in an alternative dynamic in vitro peritoneal dialysis model in which monocytes were exposed to test fluid that was continuously equilibrated with an interstitial fluid-like medium through a microporous membrane. The chemiluminescence response by stressed monocytes was also tested after an 18 h recovery period. All tests were performed during or after exposure to different degrees of glycerol induced osmotic stress and after exposure to a 1% milk-whey derived, polypeptide enriched test fluid. Cells incubated in 0.1% gel Hanks buffer (GH) served as control. RESULTS: Osmotic stress induced impairment of leucocyte function was found by the chemiluminescence assay (mean (SEM): 179 (20)% v 138 (23)% after 30 minutes in 0.5% and 1.5% glycerol, respectively) and by the analysis of IL-8 released by monocytes (44 (9) ng in 0.7% glycerol v 40 (7) ng in 2.0% glycerol). Only the chemiluminescence assay showed a protective effect of polypeptides on leucocyte function (after > or = 60 minutes). If monocytes were allowed to recover in culture medium after exposure to test fluids, the changes in chemiluminescence response appeared to be reversible after a 30 minute exposure, but became more pronounced after 60 and 120 minutes. The phagocytosis and bacterial killing assays were less sensitive. The observations carried out with the phagocytosis assay did not correspond with the Fc or C3 receptor density data. CONCLUSIONS: The release of IL-8 by peripheral blood monocytes in a two compartment model and their chemiluminescence response are appropriate assays for the assessment of changes in leucocyte function in response to different peritoneal dialysis fluids.
Dialysis Solutions↗
Metabolic activity of pulmonary endothelium: modulations of structure and function.
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Animals↗
Hemorrhage and resuscitation: immunological aspects.
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Animals↗
Phagocytosis by emigrated, intra-abdominal neutrophils is depressed during human secondary peritonitis.
The phagocytic function of neutrophils is a crucial element in host defense against invading microorganisms. Patients with diffuse peritonitis depend on adequate reactivity of neutrophils, in particular locally in the peritoneal cavity as well as in the circulation. This study examined phagocytosis as well as numerical expression of Fcgamma I-III (CD16, CD32, CD64) and complement receptors (CD18, CD35) of emigrated, intra-abdominal and circulating neutrophils during human secondary peritonitis using fluorescence-activated cell analysis. Optimally opsonized E. coli bacteria were used independently of the well-known low level of opsonic molecules during peritonitis. Compared with controls (abdominal surgery without peritonitis), the percentage of emigrated neutrophils which engulfed E. coli bacteria was significantly depressed until 48 h after diagnosis of, and surgery for, peritonitis. When patients with complicated peritonitis (septic shock, multiple organ failure) were compared with patients without complications, phagocytosis was even more depressed in patients with complications. Numerical expression of CD64 (Fcgamma RI) and CD35 (CR1) increased significantly on emigrated polymorphonuclear leukocytes (PMNs) during peritonitis when compared to controls. There was no difference in CD18 and CD32 (Fcgamma RII) expression between the two groups. Numerical expression of CD16 (Fcgamma RIII) on emigrated PMNs decreased significantly in peritonitis. This was more pronounced in patients with complicated peritonitis. We conclude that there is a long-lasting depression of phagocytosis by emigrated PMNs during peritonitis, independent of the opsonic activity. Our data suggest that decreased phagocytosis might be correlated to the profound drop in CD16 on these cells.
Abdominal Cavity↗
Signaling mutations and autoimmunity.
Mutations in a number of signaling components in mice can lead to strong autoimmune phenotypes. In some cases, these mutations likely compromise important feedback inhibitory pathways that downregulate antigen receptor signaling. For example, a deficiency of Lyn leads to a severe lupus-like autoimmunity. This autoimmunity may result from loss of a feedback inhibitory pathway in which Lyn phosphorylates CD22, triggering recruitment of the tyrosine phosphatase SHP-1 to the plasma membrane, which then dampens BCR signaling. Loss of Lyn also compromises an inhibitory pathway involving Fc gamma RIIb and SHIP, an inositol phosphatase. Mutation of Fyn exacerbates the autoimmunity caused by loss of Lyn. This may be due in part to a nonimmunological compromise in the integrity of the podocytes in the kidney, which may make the kidneys more susceptible to immune complex-induced damage. Fyn-deficient mice exhibit a number of immunological abnormalities and also exhibit some autoimmunity, although this is less severe than what is seen in Lyn-deficient mice. Recently a gain of function mutation in CD45 that may enhance activity of Src family tyrosine kinases has also been found to cause autoimmune disease, suggesting that the level of Src family tyrosine kinase activity is an important determinant of immune tolerance. Finally, several studies suggest that there is a significant interaction between Src family tyrosine kinases and the Fas pathway that is important for self-tolerance. Although these studies are still at an early stage, it seems clear that alterations in regulators of antigen receptor signaling can contribute to autoimmunity.
Animals↗
Reticulo-endothelial function in glomerulonephritis.
IgG- and C3b-coated erythrocytes were used to investigate splenic Fc-receptor function and hepatic C3b-receptor function by measurements of their blood clearance. Most patients with glomerular disease including those who were HLA, A1, B8, DR3 had normal Fc-receptor function. Occasional individuals with persistent glomerulonephritis had delayed clearance unrelated to disease activity. In rapidly progressive glomerulonephritis, the phenomenon of 'reticulo-endothelial blockade' was confirmed. C3b-receptor function was normal in most patients with persistent glomerulonephritis. A defect in splenic Fc-receptor function hepatic C3b-receptor function is unlikely to underlie persistent glomerulonephritis.
Adult↗
Phagocytosis inhibits the production of C2 by human monocytes.
Production of the second complement component by cultured human monocytes was suppressed by the addition of a variety of phagocytosable particles. The degree of suppression was related to the concentration of particles, but was unrelated to particle size, the presence of surface sialic acid, antibody or C3b. The failure to reverse suppression by prostaglandin synthetase inhibitors indicates that it is not mediated by prostaglandins.
Cells, Cultured↗
Enhancement of leukocyte membrane receptor expression after mechanical agitation.
Granulocyte and lymphocyte suspensions were exposed to slight mechanical agitation for 30 s on a tube mixer before being examined for membrane receptors by rosette techniques. Agitation caused an increase in the proportion of granulocytes bearing receptors for sheep erythrocytes (E-R), for the Fc portion of IgG (Fc gamma-R), and for C3b (C3b-R), and of lymphocytes bearing the Fc gamma-R. The proportion of E-R-bearing lymphocytes was not enhanced, with the exception of the 'early' or 'active' E-R-bearing cells. The increase in rosette formation was specific, i.e. rosette formation with ox or rabbit E was not induced by agitation. The increased proportion of membrane receptors was not associated with an increase in granulocyte phagocytosis of preopsonized zymosan particles, as measured by chemiluminescence. Membrane perturbation thus probably increases the availability of surface receptors.
Animals↗