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PubMed1994

Neutrophil-specific antigen NB1 inhibits neutrophil-endothelial cell interactions.

Neutrophil-specific antigen NB1 is located on a 58 to 64 kd glycosyl phosphatidylinositol-linked plasma membrane glycoprotein. NB1 antigen can be detected on neutrophils from 97% of healthy volunteers, and NB1 antigen is expressed on subpopulations of neutrophils. Neutrophil subpopulations with varying functions have been described, and we hypothesize that NB1 antigen may play an important role in neutrophil function. We compared the function of NB1-positive and NB1-negative neutrophils obtained from several persons. There were no differences in the adhesion of NB1-positive and NB1-negative neutrophils incubated in C5a, N-formyl-Met-Leu-Phe (FMLP), phorbol myristate acetate (PMA), or buffer to type IV collagen, fibronectin, laminin, or polystyrene. However, the adherence to human umbilical vein endothelial cells (HUVEC) monolayers of unstimulated NB1-positive neutrophils was less than to NB1-negative neutrophils (20.0% +/- 4.2% vs 31.7% +/- 5.8%; p < 0.01). When neutrophils were stimulated with C5a, PMA, or FMLP, no differences were found in the adhesion of NB1-positive and NB1-negative cells to the same surfaces. When NB1-positive neutrophils were incubated with rabbit polyclonal anti-NB1 Fab fragments, their adherence to HUVEC was increased (32.9% +/- 10.1% vs 18.3% +/- 5.0%; p < 0.05). Fab fragments prepared from normal rabbit serum had no effect on neutrophil adherence to HUVEC. The chemotaxis of NB1-positive neutrophils to FMLP through nitrocellulose was significantly greater than that of NB1-negative neutrophils (p = 0.03), but there was no difference in chemotaxis to FMLP through polycarbonate membranes.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies↗
PubMed1994

Circulating monocytes are activated in newly diagnosed type 1 diabetes mellitus patients.

Investigations in the BB rat and the non-obese diabetic (NOD) mouse have provided substantial evidence for the involvement of the monocyte/macrophage system in the development of type 1 diabetes mellitus. However, it is not known whether monocytes play the same role in the pathogenesis of human type 1 diabetes. We investigated this problem in a longitudinal study of 29 recent-onset type 1 diabetes mellitus patients. Monocyte chemotaxis, phagocytosis and superoxide production as well as metabolic and haematological parameters were studied immediately after diagnosis and 6 months later. At diagnosis the patients had activated casein and C5a chemotaxis (casein 70 +/- 9 versus 150 +/- 5 (mean +/- s.e.m.), P < 0.001; C5a 137 +/- 10 versus 158 +/- 5, P < 0.05 (activation immobilizes monocytes, reducing the measured values)), and activated superoxide production (3.6 +/- 0.3 versus 3.0 +/- 0.3, P < 0.05). After 6 months casein chemotaxis (115 +/- 16 versus 150 +/- 5, P < 0.05) and Candida phagocytosis (3.3 +/- 0.1 versus 2.8 +/- 0.2, P < 0.001) were still activated. There was no correlation with other clinical or paraclinical parameters. We conclude that the circulating monocytes in newly diagnosed type 1 diabetes patients are activated. It is reasonable to expect that monocytes at the local site of inflammation in pancreas are even further activated. This could play a pathogenic role in beta cell destruction.

Adult↗
PubMed1991

Defective polymorphonuclear leukocyte formyl peptide receptor(s) in juvenile periodontitis.

Juvenile periodontitis (JP) is a disease characterized by severe gingival infections. PMN from some JP patients exhibit abnormal chemotactic responsiveness when challenged with the synthetic formyl peptide, FMLP. While investigating PMN function in JP, we found a patient in whom abnormal PMN chemotactic responses to FMLP were associated with a defective population of PMN formyl peptide receptor(s) (FPR). JP PMN failed to respond chemotactically when challenged with FMLP, but exhibited normal chemotactic responses upon exposure to purified human C5a. Furthermore, JP PMN were capable of degranulating and generating superoxide anion radicals as well as normal PMN upon exposure to FMLP. Binding studies demonstrated that JP PMN had a diminution in the number of high-affinity FPR. Studies in which FPR was radiolabeled by chemical cross-linking demonstrated that JP PMN FPR exhibited the same molecular weight and N-linked glycosylation as normal PMN FPR. JP PMN FPR, however, was more resistant to papain cleavage than normal PMN FPR. Autoradiograms obtained from 2D-PAGE of normal and JP PMN FPR demonstrated decreased amounts of FPR isoforms in JP PMN.

Adult↗
PubMed1992

[Fundamental and clinical studies of homologous immunoglobulin-free priming in cardiopulmonary bypass, with special reference to anaphylatoxin production].

In in-vitro study, human immunoglobulin (Ig) denatured by O2 bubbling markedly produced C4a, C3a, and C5a, whereas human albumin treated identically did not. White blood cells (WBC) treated by O2 bubbling significantly increased C3a levels alone, but at a much lesser grade than the Ig. A new priming method, i.e., homologous concentrated red cell (CRC) and human albumin was discerned from the experimental facts in-vitro, and we investigated the clinical effects of that priming method. C4a, C3a and C5a in BOG primed with homologous whole blood (HWB) were slightly higher than those in MOG during CPB. Those in the Ig-free priming group were more mildly increased than those in the HWB priming group, not only during CPB, but also after protamine administration; this tendency was clearer in BOG. It is concluded that (1) human immunoglobulin (Ig) denatured by O2 bubbling produces anaphylatoxins via the classical pathway; (2) WBC treated identically produces C3a at a far milder grade; (3) priming with CRC and human albumin reduces plasma anaphylatoxin levels; and (4) pulmonary function at an early postoperative period was improved in the homologous Ig-free priming group, especially with BOG.

Albumins↗
PubMed1995

IL-1 activation of endothelium supports VLA-4 (CD49d/CD29)-mediated monocyte transendothelial migration to C5a, MIP-1 alpha, RANTES, and PAF but inhibits migration to MCP-1: a regulatory role for endothelium-derived MCP-1.

We investigated the effect of interleukin-1 (IL-1) activation of human umbilical vein endothelium (HUVE) on human monocyte transendothelial migration induced by chemotactic factors. Monocyte migration across unactivated endothelium in response to macrophage inflammatory protein-1 alpha (MIP-1 alpha), RANTES, platelet-activating factor (PAF), or monocyte chemoattractant protein-1 (MCP-1) was completely inhibited (90%) by monoclonal antibodies (mAbs; 60.3) to CD18 of the CD11/CD18 complex on the monocyte and partially inhibited (by 75%) in response to C5a. When the HUVE was stimulated with IL-1 alpha (5 h, 0.1 ng/ml), monocyte migration in response to C5a, MIP-1 alpha, RANTES, or PAF was no longer inhibited by mAb to CD18. However, migration was blocked by the combination of mAb to the alpha 4-integrin (CD49d) chain of very late antigen-4 (CD49d/CD29) with the mAb to CD18. In contrast to the above stimuli, activation of the HUVE with IL-1 alpha inhibited the transendothelial migration of monocytes in response to MCP-1. mAbs to the adhesion molecules up-regulated on HUVE by IL-1, i.e., E-selectin (CD62E), intercellular adhesion molecule-1 (CD54) or vascular cell adhesion molecule-1 (CD106), did not reverse the inhibitory effect. Transendothelial migration in response to MCP-1 but not to C5a was inhibited by the treatment of monocytes with culture supernatant from IL-1 alpha-stimulated (but not from unstimulated) HUVE. Such supernatant contained chemotactic activity for monocytes, and a mAb to MCP-1 blocked the migration inhibitory effect of IL-1 activation of the HUVE monolayer, as well as the chemotactic activity in the supernatant from IL-1-stimulated HUVE. The inhibitory effect on migration of IL-1-stimulated HUVE was specific for monocytes because polymorphonuclear leukocyte transendothelial migration in response to IL-8 (a related chemokine) was not inhibited by IL-1 activation of HUVE.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Adhesion Molecules↗
PubMed1996

Functional abnormalities in granulocytes predict susceptibility to bacterial infections in chronic lymphocytic leukaemia.

Leukocyte functions were studied in 22 patients with chronic lymphocytic leukaemia (CLL) and were related to the patients' susceptibility to infections. In CLL patients with a history of infections, compared with CLL patients without infections or healthy controls, there were significant impairments of most granulocyte functions; random migration, N-formyl-methionylleucylphenylalanine (fMLP) and C5a stimulated chemotaxis and chemiluminescence response were decreased. No differences in these functions between CLL patients without infections and healthy controls were observed. Phagocytosis and intracellular killing of granulocytes were intact in all patients with CLL. By univariate analysis, neutrophil count and serum IgG level also predicted susceptibility to infections. By multivariate analyses, granulocyte chemotaxis and chemiluminescence remained as statistically significant predictors of infections. The lymphocyte functions (mitogen-induced lymphocyte proliferation and immunoglobulin production in vitro) were equally impaired in all patients with CLL and differed significantly from the respective functions in healthy control subjects. We conclude that impairments in granulocyte functions contribute to susceptibility to infections in CLL.

Aged↗
PubMed1984

Inflammatory mediators stimulate granulocyte adherence to cultured human endothelial cells.

The factors that regulate the adherence of granulocytes to the endothelium under normal conditions, and in states of inflammatory vascular injury, are largely unknown. We found that treatment of primary, confluent monolayers of human umbilical vein endothelial cells with inflammatory mediators (zymosan-activated plasma, as a source of C5a fragments, and N-formylmethionyl-leucyl-phenylalanine) stimulated granulocyte adherence to the monolayers. The augmented adherence was dose-, time-, and temperature-related and demonstrated kinetics characteristic of the adherence of single cells with increased affinity for monolayer cultures. Adherence stimulated by the inflammatory mediators was not prevented by washing the monolayers after treatment with the mediator. Human albumin diminished both spontaneous and stimulated adherence, although the relative increase in adherence stimulated by the inflammatory mediator was unchanged. Calcium and magnesium were required for stimulated adherence. These data suggest that inflammatory mediators may bind to, or directly alter, human endothelial cells resulting in enhanced granulocyte adherence, and define characteristics of this endothelial cell-granulocyte interaction.

Cell Adhesion↗
PubMed1990

Evidence that a receptor-operated event on the neutrophil mediates neutrophil accumulation in vivo. Pretreatment of 111In-neutrophils with pertussis toxin in vitro inhibits their accumulation in vivo.

The role of neutrophil chemoattractant receptors in neutrophil stimulation in vitro is well established, however, the precise mechanisms underlying local neutrophil accumulation at inflammatory sites in vivo have not been defined. A fundamental question that remains open is whether chemoattractants act on the endothelial cell or the neutrophil to initiate the process of neutrophil migration in vivo. To address this question we have investigated whether neutrophil accumulation in vivo can occur if chemoattractant receptor occupancy is uncoupled from neutrophil stimulation. For this purpose we have used pertussis toxin (PT) as the pharmacologic tool. We have investigated the effect of in vitro pretreatment of rabbit neutrophils with PT on their responses in vitro and on their accumulation in vivo. Pretreatment of rabbit neutrophils with PT inhibited FMLP- and C5a-, but not PMA- induced increases in CD18 expression, neutrophil adherence, and degranulation in vitro. This pretreatment procedure with PT inhibited the accumulation of radiolabeled neutrophils in vivo in response to intradermally injected FMLP, C5a, C5a des Arg, leukotriene B4, IL-8, and zymosan in rabbit skin. Further, in contrast to the in vitro results, PT inhibited the PMA-induced 111In-neutrophil accumulation in vivo. Interestingly, pretreatment of neutrophils with PT also inhibited accumulation in response to intradermally injected IL-1, despite the reports that IL-1 lacks neutrophil chemoattractant activity in vitro. Although the experimental techniques used cannot distinguish the different stages of neutrophil migration involved, these results suggest that the accumulation of neutrophils induced by local extravascular chemoattractants in vivo depends on a pertussis toxin-sensitive receptor operated event on the neutrophil itself. Further, PMA and IL-1 may release secondary chemoattractants in vivo.

Animals↗
PubMed1989

Heteronuclear three-dimensional NMR spectroscopy of the inflammatory protein C5a.

The utility of three-dimensional heteronuclear NMR spectroscopy for the assignment of 1H and 15N resonances of the inflammatory protein C5a (MW 8500), uniformly labeled with 15N, is demonstrated at a protein concentration of 0.7 mM. It is shown that dramatic simplification of the 2D nuclear Overhauser effect spectrum (NOESY) is obtained by editing with respect to the frequency of the 15N heteronucleus in a third dimension. The improved resolution in the 3D experiment largely facilitates the assignment of protein NMR spectra and allows for the determination of distance constraints from otherwise overlapping NOE cross peaks for purposes of 3D structure determination. The results show that 15N heteronuclear 3D NMR can facilitate the structure determination of small proteins and promises to be a useful tool for the study of larger systems that cannot be studied by conventional 2D NMR techniques.

Amino Acid Sequence↗
PubMed1990

Recombinant C5a stimulates transcription rather than translation of interleukin-1 (IL-1) and tumor necrosis factor: translational signal provided by lipopolysaccharide or IL-1 itself.

We investigated the effects of recombinant C5a (rC5a) on gene expression and synthesis of interleukin-1 beta (IL-1 beta) and tumor necrosis factor (TNF) in fresh human peripheral blood mononuclear cells (PBMC). Total (cell-associated and secreted) cytokine synthesis was measured. In the strict absence of endotoxin (lipopolysaccharide [LPS]), rC5a resulted in a small but statistically insignificant increase in immunoreactive IL-1 beta and TNF, as well as in IL-1 and IL-6 bioactivity. On the other hand, rC5a induced marked transcriptional activation of IL-1 beta and TNF in a dose-dependent fashion with an optimal concentration of 50 ng/mL. The rC5a-induced cytokine messenger RNA (mRNA) was not spontaneously translated into protein. At 50 ng/mL, rC5a induced the same levels of mRNA for IL-1 beta and TNF as 1 ng/mL of LPS, whereas LPS induced 12 times more IL-1 beta protein and 70 times more TNF protein than rC5a alone. The C5a-induced mRNA half-life was the same as that induced by LPS. Formyl-Meth-Leu-Phe (fMLP) did not induce cytokine transcription. Pretreatment with rC5a enhanced cytokine synthesis induced by other stimuli. After 2 hours of preincubation with rC5a, PBMC synthesized 3 to 10 times more IL-1 beta and TNF on subsequent stimulation by LPS or IL-1 itself. We conclude that rC5a provides primarily a transcriptional but not translational signal for IL-1 beta and TNF; the half-life of the untranslated mRNA is the same as that of translated message; rC5a-induced transcription upregulates PBMC for enhanced synthesis of these cytokines; and a translational signal can be provided by LPS or IL-1 itself.

Complement C5a↗
PubMed1981

A monoclonal antibody-inhibiting FMLP-induced chemotaxis of human neutrophils.

A monoclonal IgG1 antibody, termed NCD3, was raised against human neutrophils and has been shown to inhibit neutrophil chemotaxis. NCD3 displayed a considerable degree of stimulus specificity in that it inhibited N-formyl-methionyl-leucyl-phenylalanine- (FMLP) induced chemotaxis up to 80%, C5a and zymosan-activated plasma induced chemotaxis by only 20% and had no effect on leukotriene B4- (LTB4) or casein-mediated chemotaxis. NCD3 did not inhibit granule enzyme release from neutrophils in response to stimulation by various secretagogues, including FMLP, in the presence or absence of cytochalasin B (CB). Neutrophil phagocytosis of 51Cr-labeled opsonized sheep erythrocytes (51Cr-EAC) and superoxide anion (O2-) production in response to FMLP or phorbol myristate acetate (PMA) stimulation were not affected by pretreating cells with NCD3. Divalency of NCD3 was necessary for inhibition of chemotaxis, suggesting a requirement for cross-linking of the antigenic determinants on the neutrophil membrane surface.

Anaphylatoxins↗
PubMed1993

Diversity in regulation of adhesion molecules (Mac-1 and L-selectin) in monocytes and neutrophils from neonates and adults.

The surface expression and regulation of the adhesion promoting glycoproteins Mac-1 and L-selectin was measured on monocytes and neutrophils from neonates and adults. A significant decrease in Mac-1 up regulation on both monocytes and neutrophils was found in neonates after both high (10(-7)M) and low (10(-9)M) concentrations of the chemotactic factor N-formyl-methionyl-phenylalanine (FMLP). A significant difference was obtained after incubation for five minutes, which was further enhanced after incubation for 15 minutes. Factors related to bacterial infections, lipopolysaccharides, activated sera (C5a), and aggregated IgG induced an impaired Mac-1 up regulation on both monocytes and neutrophils from neonates compared with adults. The expression of L-selectin was significantly lower on neutrophils from neonates and was less down regulated upon stimulation with a low concentration (10(-12)M) of FMLP. On monocytes from neonates, the expression and down regulation of L-selectin did not differ from monocytes from adults. Mode of delivery did not influence the regulation of Mac-1 and L-selectin in neonates. Diversity in expression and regulation of Mac-1 and L-selectin on monocytes and neutrophils may contribute to the increased susceptibility to infections observed in neonates.

Adolescent↗
PubMed1999

The MultiScreen filtration system to measure chemoattractant-induced release of leukocyte granule enzymes by differentiated HL-60 cells or normal human monocytes.

A variety of chemoattractants initiate chemotaxis by selective binding to chemoattractant receptors (CARs), a subfamily of seven transmembranous G-protein coupled receptors (7TM-GPCRs) expressed in the leukocyte plasma membrane. Whatever the chemoattractant, signaling leading to chemotaxis involves several common biological steps which occur within seconds to minutes of CAR ligand binding. Though each step can be used to study the progress of the chemotaxis activation process. only certain biological events are suitable for monitoring chemotaxis signaling on large sample numbers as required for drug screening. An example of such is the release of granule enzymes by leukocytes in response to a CAR ligand. In this study, promyelocytic HL-60 cells were employed to set up a 96-well microplate methodology using filtration instead of centrifugation to collect the extracellular fluid together with the cell-released enzymes. Undifferentiated HL-60 cells were found not to respond to any of the CAR ligands. With various types of HL-60 cells which had differentiated along the neutrophilic or monocytic pathways, a large enzyme release was dose-dependently triggered by fMLF or C5a, but none of the tested CC or CXC chemokines. The highest responsiveness was found for neutrophilic HL-60 cells differentiated with dibutyryl cyclic AMP. With normal human monocytes (prepared from the blood of healthy donors by leukapheresis and elutriation), the granule enzyme release response was large to fMLF or C5a, substantial to MCP-1, low to RANTES or MIP-1alpha, but insignificant to Eotaxin, IL-8 and GROalpha. The method readily measures N-acetyl-beta-D-glucosaminidase, beta-D-glucuronidase and elastase activities, and requires approximately five times fewer cells than classical methods, a very important feature when normal human cells are to be used in screening assays. The method was also adapted to large scale screening of antagonists such as cyclosporins A and H for fMLF-mediated signaling using HL-60 cells and monocytes, and truncated (9-76) MCP-1 for MCP-1-mediated signaling using monocytes.

Cell Differentiation↗
PubMed2005

TNF-alpha promotes a stop signal that inhibits neutrophil polarization and migration via a p38 MAPK pathway.

Neutrophils are a major component of the inflammatory response in patients with asthma and other inflammatory conditions. Proinflammatory cytokines, such as tumor necrosis factor alpha (TNF-alpha), are increased in the airway of patients with severe asthma and have been implicated in the recruitment of neutrophils into areas of inflammation. Here, we show that TNF-alpha induces a stop signal that promotes firm neutrophil adhesion and inhibits neutrophil polarization and chemotaxis to chemoattractants including interleukin-8 and C5a. TNF-alpha treatment of neutrophils plated on a fibrinogen-coated surface promotes firm neutrophil adhesion and the formation of vinculin-containing focal complexes. TNF-alpha induces a more than tenfold increase in p38 mitogen-activated protein kinase (MAPK) but not extracellular signal-regulated kinase phosphorylation. Inhibition of p38 MAPK in neutrophils treated with TNF-alpha causes neutrophil polarization and motility. These findings suggest that TNF-alpha initiates a stop signal through a p38 MAPK pathway, which may promote the retention of neutrophils in inflammatory sites. Together, our data suggest that inhibition of p38 MAPK may be an attractive target to limit inflammatory responses that are mediated by TNF-alpha.

Asthma↗
PubMed1998

[Prediction of rehabilitation outcome after surgical interventions based on biochemical parameters: a new concept in mediator research].

The perioperative changes in epinephrin-, norepinephrine-, histamin-, C5a- and interleukin-6-levels were studied in 40 patients undergoing cholecystectomy for the diagnosis of acute cholecystitis. All relevant mediator levels could be determined in 38 patients. The outcome was not optimal in 16 of them (42%). In order to evaluate the predictive value of the mediators under investigation for the quality of the patients' outcome, a model based on the Bayes' theorem was developed. Using this model the outcome (optimal vs. not optimal) could be correctly predicted in 30 (79%) of our study patients. This kind of data analysis allows to define states of increased risk for a not optimal recovery based on biochemical parameters.

Acute Disease↗
PubMed1995

Migration of dendritic cells in response to formyl peptides, C5a, and a distinct set of chemokines.

Trafficking to tissues and then to lymph nodes is a crucial aspect of the immunobiology of dendritic cells. The present study was designed to identify molecules able to direct the migration of human blood-derived dendritic cells. fMLP (representative of formyl peptides of bacterial origin), C5a, and the C-C chemokines monocyte chemotactic protein (MCP)-3, MIP-1 alpha/LD78, and RANTES elicited chemotactic migration and a rise of intracellular free calcium in dendritic cells. In contrast, the C-X-C chemokines IL-8 and IP-10 and the C-C chemokines MCP-1 and MCP-2 were inactive as chemoattractants. Thus, dendritic cells respond to classical chemotactic signals and to a set of chemokines distinct from that active on monocytes and neutrophils. Chemoattractants are likely to contribute to localization and trafficking of dendritic cells and provide tools to recruit these cells in the design of immunization strategies.

Calcium↗
PubMed1993

Effects of adenosine and its analogues on actin polymerization in human polymorphonuclear leucocytes.

1. The effects of adenosine and its analogues on actin polymerization in human polymorphonuclear leucocytes (PMN) induced by three different chemotactic stimulants, platelet-activating factor (PAF), N-formyl-methionyl-leucyl-phenylalanine (FMLP) and an activated fragment of C5 (C5a) were investigated. 2. Adenosine and its analogues inhibited the actin polymerization induced by these three agents in a concentration-dependent manner and theophylline, a competitive antagonist at adenosine receptors, abolished these inhibitory effects. 3. The adenosine analogue 5'-N-ethylcarboxamideadenosine (NECA) was a more potent inhibitor of actin polymerization than either L-N6-phenylisopropyladenosine (PIA) or adenosine itself; the rank order of potency of these agonists was characteristic of adenosine A2 receptors. 4. Adenosine deaminase (ADA) abolished the inhibitory effect of adenosine and augmented PAF-induced actin polymerization. 5. It was concluded that, at physiological concentrations, adenosine inhibits actin polymerization in PMN via activation of PMN surface membrane adenosine A2 receptors and thus modulates chemotactic stimulus-induced PMN motility.

Actins↗
PubMed1983

Newborn polymorphonuclear leukocyte aggregation: a study of physical properties and ultrastructure using chemotactic peptides.

N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) and N-formyl-L-methionyl-L-phenylalanine (FMP) were used to investigate neutrophil (PMN) aggregation. Neutrophils were isolated from healthy adult volunteers and term newborn cord blood. Neutrophil aggregation was measured after the addition of FMLP and FMP. Adult PMN aggregation curves demonstrated initial aggregation with slow deaggregation. Newborn neutrophil aggregation curves showed slow aggregation with no deaggregation. These results were identical to the adult and newborn neutrophil aggregation curves produced by C5a. Newborn PMN aggregates examined by scanning electromicrography showed frequent, dense aggregates compared with fewer, less dense aggregates of adult PMNs. Adult and newborn PMN aggregates differed when compared by transmission electromicrographs (EM). Newborn PMNs were tightly bound with cell membrane projections; adult PMNs were loosely bound with no cell membrane projections. Cytochalasin-B pretreated adult and newborn PMN aggregates displayed close approximation of cell membranes with large numbers of cytoplasmic projections. Newborn neutrophils are irreversibly aggregated by FMLP and FMP whereas adult neutrophils display an aggregation-deaggregation reaction. EM studies suggest that this irreversible aggregation of untreated newborn neutrophils may differ from the irreversible aggregation of cytochalasin-B pretreated neutrophils.

Adult↗