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1
Leino, Lasse, and Max J. Paape. "Comparison of the chemiluminescence responses of bovine neutrophils to differently opsonized zymosan particles." American Journal of Veterinary Research 54, no. 7 (July 1, 1993): 1055–59. http://dx.doi.org/10.2460/ajvr.1993.54.07.1055.
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Summary Stimulatory effects of 6 zymosan preparations on luminol-dependent chemiluminescence (cl) responses of isolated bovine neutrophils were compared. Unopsonized zymosan particles and zymosan particles opsonized with bovine IgG1, IgG2, fresh serum, or serum from which zymosan-specific antibodies, but not complement, had been removed (C3-serum) induced strong cl responses, with nearly equal maximal peaks in the presence of extracellular Ca2+ and Mg2+, whereas the response to fetal bovine serum-opsonized zymosan particles was markedly low. Removal of extracellular divalent cations almost completely blocked the cl reaction triggered by unopsonized, IgG1-opsonized, C3-opsonized, and fetal bovine serum-opsonized zymosan particles. By contrast, no change in the respiratory burst activity induced by serum-opsonized zymosan and only partial reduction in the response to IgG2-opsonized zymosan were seen under these conditions. Further experiments were performed with 4 zymosan preparations on neutrophils isolated from 2 calves with a genetic deficiency of CD11/CD18 membrane antigens. The unopsonized zymosan-induced cl reaction was absent in these cells. A reduced, but clear, response was observed with C3-opsonized zymosan. Unexpectedly, in the absence of extracellular Ca2+ and Mg2+, serum-opsonized zymosan failed to generate the respiratory burst, whereas response to IgG2-opsonized zymosan was normal in the CD11/CD18-deficient neutrophils. These findings indicate that unopsonized zymosan may act in a divalent cation-dependent manner at the receptor for C3bi in bovine neutrophils, as it has been shown to do in the human system. In addition, it seems that IgG2-Fc receptors capable of signaling the respiratory burst in the absence of extracellular Ca2+ and Mg2+ exist on bovine neutrophils.
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Remold-O'Donnell, E., and D. Parent. "Downregulation of neutrophil CD43 by opsonized zymosan." Blood 85, no. 2 (January 15, 1995): 337–42. http://dx.doi.org/10.1182/blood.v85.2.337.337.
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Abstract CD43, a prevalent white blood cell molecule distinguished by its mucin- like surface region, has been proposed as a “functional barrier” that prevents or negatively regulates a variety of cell surface interactions. Implicit in this hypothesis is the expectation that CD43 will be altered or removed when white blood cells are activated. To investigate alterations of CD43 in a dramatic example of functional cell activation, suspension neutrophils were challenged with opsonized zymosan, a characterized stimulator of phagocytosis and respiratory burst oxidase. Flow cytometry showed decreased surface density of CD43 in opsonized zymosan-treated neutrophils, and immune precipitation showed decreased cellular CD43 content, indicating that opsonized zymosan downregulates CD43 by a proteolytic mechanism. Based on densitometry of immune precipitates, CD43 levels were decreased 42% +/- 6% in neutrophils treated for 10 minutes with opsonized zymosan and decreased 70% +/- 3% in neutrophils treated with phorbol 12-myristate 13-acetate (PMA). CD43 downregulation in response to opsonized zymosan, like PMA-induced CD43 downregulation, was insensitive to the serine protease inhibitor diisopropylfluorophosphate (DFP). In contrast, CD43 downregulation in response to opsonized zymosan or PMA was prevented by 4-(2-aminoethyl)-benzenesulfonylfluoride (AEBSF) and 3′4′- dichloroisocoumarin (3,4-DCI), both of which are characterized serine protease inhibitors. Activation of the neutrophil respiratory burst oxidase by opsonized zymosan or PMA was also insensitive to DFP and prevented by AEBSF and 3,4-DCI. These findings indicate a requirement for a proteolytic step in activation of the respiratory burst of intact suspension neutrophils by opsonized zymosan and PMA and suggest that CD43 cleavage may be a required proteolytic event.
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Remold-O'Donnell, E., and D. Parent. "Downregulation of neutrophil CD43 by opsonized zymosan." Blood 85, no. 2 (January 15, 1995): 337–42. http://dx.doi.org/10.1182/blood.v85.2.337.bloodjournal852337.
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CD43, a prevalent white blood cell molecule distinguished by its mucin- like surface region, has been proposed as a “functional barrier” that prevents or negatively regulates a variety of cell surface interactions. Implicit in this hypothesis is the expectation that CD43 will be altered or removed when white blood cells are activated. To investigate alterations of CD43 in a dramatic example of functional cell activation, suspension neutrophils were challenged with opsonized zymosan, a characterized stimulator of phagocytosis and respiratory burst oxidase. Flow cytometry showed decreased surface density of CD43 in opsonized zymosan-treated neutrophils, and immune precipitation showed decreased cellular CD43 content, indicating that opsonized zymosan downregulates CD43 by a proteolytic mechanism. Based on densitometry of immune precipitates, CD43 levels were decreased 42% +/- 6% in neutrophils treated for 10 minutes with opsonized zymosan and decreased 70% +/- 3% in neutrophils treated with phorbol 12-myristate 13-acetate (PMA). CD43 downregulation in response to opsonized zymosan, like PMA-induced CD43 downregulation, was insensitive to the serine protease inhibitor diisopropylfluorophosphate (DFP). In contrast, CD43 downregulation in response to opsonized zymosan or PMA was prevented by 4-(2-aminoethyl)-benzenesulfonylfluoride (AEBSF) and 3′4′- dichloroisocoumarin (3,4-DCI), both of which are characterized serine protease inhibitors. Activation of the neutrophil respiratory burst oxidase by opsonized zymosan or PMA was also insensitive to DFP and prevented by AEBSF and 3,4-DCI. These findings indicate a requirement for a proteolytic step in activation of the respiratory burst of intact suspension neutrophils by opsonized zymosan and PMA and suggest that CD43 cleavage may be a required proteolytic event.
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Elstad, M. R., C. J. Parker, F. S. Cowley, L. A. Wilcox, T. M. McIntyre, S. M. Prescott, and G. A. Zimmerman. "CD11b/CD18 integrin and a beta-glucan receptor act in concert to induce the synthesis of platelet-activating factor by monocytes." Journal of Immunology 152, no. 1 (January 1, 1994): 220–30. http://dx.doi.org/10.4049/jimmunol.152.1.220.
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Abstract We determined the mechanism by which opsonized zymosan particles, which are derived from yeast and composed of carbohydrate polymers, stimulate platelet-activating factor (PAF) synthesis by monocytes. A role for CD11b/CD18 was demonstrated because antibodies to this integrin decreased PAF synthesis, zymosan bearing only a ligand for CD11b/CD18 (iC3b) induced the synthesis of PAF, and monocytes that did not express CD11b/CD18 produced much less PAF than control monocytes. Ligation of CD11b/CD18 was not sufficient for PAF synthesis suggesting that an additional receptor was involved. Monocytes are known to bind beta-glucan which is a major component of zymosan. Opsonized beta-glucan particles stimulated the synthesis of PAF, and a soluble form of beta-glucan partially inhibited PAF synthesis in response to opsonized zymosan. Two lines of evidence suggested that the beta-glucan receptor mediating this response was distinct from CD11b/CD18. First, CD11b/CD18-deficient monocytes produced PAF when stimulated by zymosan opsonized with isolated C3b, a molecule that binds to complement receptor type 1 (CD35). Second, inducing contact of monocytes with zymosan by centrifugation resulted in PAF synthesis that was not inhibited by antibodies to CD11b/CD18. The combination of soluble beta-glucan and antibodies to CD11b/CD18 completely blocked PAF synthesis in response to opsonized zymosan. Together, these results demonstrate that induction of maximal PAF synthesis by serum-opsonized zymosan requires the concerted interactions of monocyte receptors for iC3b and beta-glucan. Additionally, they suggest that CD11b/CD18 facilitates binding of the particle and that a beta-glucan receptor transduces the activation signal.
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Barkov, S. Y., Y. I. Shilov, and S. Y. Shilov. "The effect of dehydroepiandrosterone on oxygen-dependent microbicidal activity of blood leukocytes in zymosan peritonitis in old rats." Russian Journal of Immunology 28, no. 1 (December 23, 2024): 19–24. https://doi.org/10.46235/1028-7221-16993-teo.
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The purpose of the present work was to study effects of dehydroepiandrosterone (DHEA) on the oxygen-dependent microbicidal activity of blood leukocytes. The studies were performed on male white nonlinear rats aged 3-6 months (young rats) and adult animals over 1.5 years old (old rats) using an experimental model of zymosan peritonitis. DHEA was administered subcutaneously to old animals on the daily basis (a total of 4 injections of 2 mg/kg body weight, the last injection 24 hours before the end of the experiment). Rats of similar age served as controls and received DHEA solvent (officinal olive oil) according to the same time regimen. 12 hours before the end of the experiment, the animals were administered a sterile suspension of zymosan A intraperitoneally at a dose of 50 mg/kg. The oxygen-dependent microbicidal activity of blood leukocytes was assessed by luminol-dependent chemiluminescence using opsonized and non-opsonized zymosan at concentrations of 15 μg/mL, 150 μg/mL and 1500 μg/mL. In old male rats, compared to young ones, the chemiluminescence indexes showed a statistically significant increase when blood leukocytes were stimulated with both opsonized and non-opsonized zymosan. Administration of DHEA to old male rats leads to a pronounced decrease in chemiluminescence in samples at all concentrations of opsonized zymosan. When leukocytes of old animals are stimulated with non-opsonized zymosan in vitro, a statistically significant increase in the production of reactive oxygen species was observed, being more pronounced at lower concentrations of inducing agent (15 μg/mL and 150 μg/mL). Meanwhile, this effect was canceled at high concentrations of zymosan. The level of spontaneous chemiluminescence, reflecting in vivo cell activation, was higher in old rats treated with DHEA compared to young animals. The direction of changes in the production of reactive oxygen species in samples with low concentrations of the in vitro activation was similar to the effects of DHEA in old rats tested for spontaneous chemiluminescence. In general, our studies confirm the pronounced immunomodulatory activity of DHEA. In general, we have found that aging of male rats leads to pronounced pro-inflammatory activation of reactive oxygen species produced by blood leukocytes at the peak of inflammation induced by zymosan injections. Administration of DHEA to old male rats significantly reduced the production of reactive oxygen species by blood leukocytes, when the cells were in vitro activated by opsonized zymosan, but stimulates production of oxygen radicals in the samples without zymosan, as well as upon exposition to non-opsonized zymosan at concentrations of 15 μg/mL and 150 μg/ mL.
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Melnick, D. A., W. M. Nauseef, S. D. Markowitz, J. P. Gardner, and H. L. Malech. "Biochemical analysis and subcellular localization of a neutrophil-specific antigen, PMN-7, involved in the respiratory burst." Journal of Immunology 134, no. 5 (May 1, 1985): 3346–55. http://dx.doi.org/10.4049/jimmunol.134.5.3346.
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Abstract The adherence of serum-opsonized yeast to neutrophils results in phagocytosis of these particulate stimuli and activation of the respiratory burst. Both events are mediated or modulated in part by the surface receptors for IgG and complement. The link between the binding of complex particulate stimuli to the cell surface, and the triggering of these neutrophil functions, is not completely understood. We have previously described an anti-human neutrophil, murine monoclonal antibody PMN7C3, which specifically inhibits the respiratory burst of neutrophils stimulated with serum-opsonized yeast. In the present study, we show that the antigen recognized by PMN7C3 (PMN7 antigen) is present on a number of neutrophil proteins, including the recently described group of related leukocyte membrane glycoproteins CR3, LFA-1, and p150,95. The PMN-7 antigen differs from other antigens associated with the C3bi receptor complex (MAC 1, MO 1, OKM1, OKM10) in that it is present only on neutrophils among peripheral blood cells. Furthermore, the binding of PMN7C3 to the neutrophil surface inhibits the activation of the respiratory burst by serum opsonized zymosan without affecting phagocytosis of these particulate stimuli. The cross-linking of cell surface PMN7 antigen by multivalent antibody is associated with the capping and internalization of antigen-antibody complexes, and appears to be necessary for the expression of maximum inhibition of opsonized zymosan-triggered respiratory burst activity. PMN7C3 also binds to a group of granule-associated proteins biochemically distinct from CR3, LFA-1, and p150,95. These granule-associated proteins containing PMN7 antigen can be mobilized to the cell surface with secretion. PMN7 antigen-bearing proteins may play a role in modulating the activation of the respiratory burst associated with phagocytosis of serum-opsonize zymosan.
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Shi, Yuhong, Yumi Tohyama, Tomomi Kadono, Jinsong He, S. M. Shahjahan Miah, Ryoichi Hazama, Chisato Tanaka, Kaoru Tohyama, and Hirohei Yamamura. "Protein-tyrosine kinase Syk is required for pathogen engulfment in complement-mediated phagocytosis." Blood 107, no. 11 (June 1, 2006): 4554–62. http://dx.doi.org/10.1182/blood-2005-09-3616.
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AbstractThe protein tyrosine kinase Syk plays a central role in Fcγ receptor–mediated phagocytosis in the adaptive immune system. We show here that Syk also plays an essential role in complement-mediated phagocytosis in innate immunity. Macrophage-like differentiated HL60 cells and C3bi-opsonized zymosan comprised the pathogen-phagocyte system. C3bi-opsonized zymosan particles promptly attached to the cells and were subsequently engulfed via complement receptor 3. During this process, Syk became tyrosine phosphorylated and accumulated around the nascent phagosomes. The transfer of Syk-siRNA or dominant-negative Syk (DN-Syk) into HL60 cells resulted in impaired phagocytosis. Quenching assays using fluorescent zymosan revealed that most of the attached zymosan particles were located inside parental HL60 cells, whereas few were ingested by the mutant cells. These data indicated that Syk is required for the engulfment of C3bi-opsonized zymosan. During C3bi-zymosan–induced phagocytosis, actin accumulation occurred around phagosomes and was followed by depolymerization, and further RhoA was activated together with tyrosine phosphorylation of Vav. These responses including the actin remodeling were suppressed in Syk-siRNA– or DN-Syk–expressing cells. Our results demonstrated that Syk plays an indispensable role in complement-mediated phagocytosis by regulating both actin dynamics and the RhoA activation pathway and that these functions of Syk lead to phagosome formation and pathogen engulfment.
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Amar, M., N. Amit, JY Scoazec, C. Pasquier, C. Babin-Chevaye, TP Huu, and J. Hakim. "K562 cells produce an anti-inflammatory factor that inhibits neutrophil functions in vivo." Blood 80, no. 6 (September 15, 1992): 1546–52. http://dx.doi.org/10.1182/blood.v80.6.1546.1546.
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Abstract We have previously reported that K562, a chronic myelogenous leukemia cell line, releases a low molecular weight factor (6 to 8 Kd) that inhibits human polymorphonuclear neutrophil (PMN) adherence and adherence-related functions tested in vitro. We now report that this factor, which we have named K562 inhibitory factor (K562-IF), has potent anti-inflammatory activity in mice, associated with an inhibition of PMN functions. Its in vitro actions were less marked with mouse PMN than with human PMN. They included (1) an inhibition of both nonstimulated locomotion and locomotion induced by FMLP or serum; (2) an inhibition of the chemiluminescence induced by opsonized zymosan, but not that induced by phorbol myristate acetate or FMLP; (3) an inhibition of the degranulation stimulated by opsonized zymosan, as reflected by lactoferrin and lysozyme release; and (4) a decrease in arachidonic acid release and leukotriene B4 production by A23187- stimulated PMN. The in vivo actions of K562-IF after intraperitoneal injection included (1) an inhibition of subcutaneous PMN accumulation at the site of injection of opsonized zymosan (PMN accumulated neither outside the vessels nor intravascularly, as shown by means of histochemistry); (2) an inhibition of neutrophil accumulation in the peritoneum of mice having received sodium caseinate or opsonized zymosan intraperitoneally; and (3) lysozyme concentration in neutrophils having reached the peritoneum after opsonized zymosan treatment equal to that in blood, suggesting diminished release. PMN influx and degranulation in the peritoneum were reduced by 50% after 3 hours of treatment with 1 microgram of K562-IF (equivalent to the effect of 120 micrograms of prednisolone). Taken together, these results show that K562-IF is a potent anti-inflammatory agent that acts by inhibiting PMN functions.
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Amar, M., N. Amit, JY Scoazec, C. Pasquier, C. Babin-Chevaye, TP Huu, and J. Hakim. "K562 cells produce an anti-inflammatory factor that inhibits neutrophil functions in vivo." Blood 80, no. 6 (September 15, 1992): 1546–52. http://dx.doi.org/10.1182/blood.v80.6.1546.bloodjournal8061546.
Full textAbstract:
We have previously reported that K562, a chronic myelogenous leukemia cell line, releases a low molecular weight factor (6 to 8 Kd) that inhibits human polymorphonuclear neutrophil (PMN) adherence and adherence-related functions tested in vitro. We now report that this factor, which we have named K562 inhibitory factor (K562-IF), has potent anti-inflammatory activity in mice, associated with an inhibition of PMN functions. Its in vitro actions were less marked with mouse PMN than with human PMN. They included (1) an inhibition of both nonstimulated locomotion and locomotion induced by FMLP or serum; (2) an inhibition of the chemiluminescence induced by opsonized zymosan, but not that induced by phorbol myristate acetate or FMLP; (3) an inhibition of the degranulation stimulated by opsonized zymosan, as reflected by lactoferrin and lysozyme release; and (4) a decrease in arachidonic acid release and leukotriene B4 production by A23187- stimulated PMN. The in vivo actions of K562-IF after intraperitoneal injection included (1) an inhibition of subcutaneous PMN accumulation at the site of injection of opsonized zymosan (PMN accumulated neither outside the vessels nor intravascularly, as shown by means of histochemistry); (2) an inhibition of neutrophil accumulation in the peritoneum of mice having received sodium caseinate or opsonized zymosan intraperitoneally; and (3) lysozyme concentration in neutrophils having reached the peritoneum after opsonized zymosan treatment equal to that in blood, suggesting diminished release. PMN influx and degranulation in the peritoneum were reduced by 50% after 3 hours of treatment with 1 microgram of K562-IF (equivalent to the effect of 120 micrograms of prednisolone). Taken together, these results show that K562-IF is a potent anti-inflammatory agent that acts by inhibiting PMN functions.
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Wolf, H. M., J. W. Mannhalter, H. C. Salzmann, J. Göttlicher, R. Ahmad, and M. M. Eibl. "Phagocytosis of serum-opsonized zymosan down-regulates the expression of CR3 and FcRI in the membrane of human monocytes." Journal of Immunology 141, no. 10 (November 15, 1988): 3537–43. http://dx.doi.org/10.4049/jimmunol.141.10.3537.
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Abstract The effect of iC3b receptor (CR3)-mediated phagocytosis on the expression of CR (C3b receptor, CR3) and IgG FcR (FcRI, FcRII) has been investigated by using serum-opsonized zymosan as a multivalent ligand for CR3. Sixteen hours after a short (1-h) pretreatment of human monocyte monolayers with zymosan opsonized with human AB serum (250 micrograms/ml), CR3 expression (as assessed by flow cytometric analysis with mAb Mo1) was significantly reduced by 59 +/- 3% (mean +/- SEM, n = 15, p less than 0.001). Concomitant with CR3 down modulation, FcR binding activity (as assessed by binding of IgG-coated E) was also found to be decreased to 41 +/- 4% of control (n = 7, p less than 0.001). Reduced FcR function was paralleled by a decrease in the expression of FcRI (as assessed with mAb 32.2). This FcRI modulation was not caused by zymosan-bound IgG because zymosan opsonized with agammaglobulinemic serum equally down regulated CR3 and FcRI expression. Pretreatment with zymosan opsonized with human AB serum, however, did not change the expression of other IgG and C-binding sites such as FcRII (examined with mAb IV.3 and 2E1) and CR1 (assessed with mAb 57F) as well as of unrelated cell membrane structures (beta 2m, MHC class II). In contrast, co-modulation for FcR function and CR3 expression induced by polymeric IgG is accompanied by a decreased expression of FcRII. These data indicate that interaction of a specific receptor with its ligand not only changes the expression of the receptor triggered, but has also a modulating effect on other receptor systems on the same cell.
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Tohyama, Yumi, Yuhong Shi, Kaoru Tohyama, and Hirohei Yamamura. "A Role of the Protein Tyrosine Kinase, Syk in Complement-Mediated Phagocytosis: A Mechanism on the Engulfment of Pathogen." Blood 106, no. 11 (November 16, 2005): 3076. http://dx.doi.org/10.1182/blood.v106.11.3076.3076.
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Abstract A protein-tyrosine kinase, Syk plays a central role in Fc-gamma receptor-mediated phagocytosis in the adaptive immune system. Here we show that Syk also makes an essential role in compliment-mediated phagocytosis in innate immunity. For this purpose, HL60 cells induced to macrophage-like with vitamin D3 and TPA and C3bi-opsonized zymosan were used as the pathogen-phagocyte system. Time-lapse microscopic observation revealed that C3bi-opsonized zymosan particles were promptly attached to and sucked into the cells but non-opsonized zymosan was not, and therefore it was indicated that our phagocytosis system is mediated by the complement receptor 3 (CR3). Syk was tyrosine-phosphorylated by the treatment with C3bi-opsonized zymosan and marked accumulation of Syk was detected around the newly forming phagosomes. To further investigate the effect of Syk on complement-mediated phagocytosis, Syk-siRNA or dominant-negative Syk (DN-Syk) was introduced into HL60 cells. Quantitative analysis by flow cytometry showed that phagocytosis was severely impaired in DN-Syk or Syk-siRNA expressing HL60 cells. To determine whether the impaired capture of zymosan is due to reduced binding to CR3 or reduced engulfment after binding, the cells were treated with a quenching reagent which discriminates fluorescent zymosan particles between inside and outside the cells. In the parental HL60 cells most of the attached zymosan particles were inside the cells, while few particles were ingested in the case of DN-Syk or Syk-siRNA expressing HL60 cells. These data indicated that Syk is required for engulfment of C3bi-opsonized zymosan but not for attachment of zymosan to CR3. To clarify the molecular mechanism how Syk affects the phagosome formation and its engulfment, the behavior of F-actin was searched microscopically. At the early stage of complement-mediated phagocytosis, marked accumulation of F-actin occurred around each phagosome and was followed by rapid depolymerization in the parental HL60 cells. In contrast, phagosomes surrounded by the accumulated actin were significantly decreased in DN-Syk or Syk-siRNA expresssing cells. These results indicate that Syk promotes actin assembly around phagosomes prior to engulfment at the early stage of the phagocytosis. As for the analysis of the downstream pathway of Syk in our phagocytosis system, RhoA-signaling was investigated. Vav-RhoA pathway was activated in HL60 cells but transfer of DN-Syk or Syk-siRNA into HL60 cells reduced the activation of Vav-RhoA signaling. Therefore Syk may act as an activator of the RhoA-pathway in phagocytosis. Our results demonstrate that Syk is required for complement-mediated phagocytosis by regulating both actin accumulation around phagosomes and RhoA-signaling harmonically and finally leads to phagosome formation and its engulfment.
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Hickstein, DD, RM Locksley, PG Beatty, A. Smith, DM Stone, and RK Root. "Monoclonal antibodies binding to the human neutrophil C3bi receptor have disparate functional effects." Blood 67, no. 4 (April 1, 1986): 1054–62. http://dx.doi.org/10.1182/blood.v67.4.1054.1054.
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Abstract Three monoclonal antibodies (MAb)--OKMI, 7C3, and 60.3-- immunoprecipitated a common 170-kd neutrophil membrane antigen closely associated with, or identical to, the C3bi receptor (CR3). Despite binding to a common receptor, these antibodies displayed marked differences in their effects on C3bi-mediated neutrophil function as assessed by the binding and ingestion of opsonized zymosan and the subsequent triggering of the respiratory burst. Antibody 7C3 caused a time-dependent, irreversible inhibition of the neutrophil oxidative response to opsonized zymosan that correlated with capping of the bound antibody. In contrast, antibody 60.3 caused an immediate inhibition of the neutrophil oxidative response to opsonized zymosan that required the continuous presence of exogenous antibody to achieve the maximal inhibitory effect. Antibody OKMI demonstrated minimal inhibition of O2- release. Despite their functional differences, binding of either 7C3 or 60.3 led to up-regulation of new antigen, presumably from intracellular sites as previously described using OKMI. Crossed immunoprecipitations of radiolabeled neutrophil lysates indicated that each MAb bound to different antigens near or within the CR3 complex. Thus three MAb binding to the neutrophil CR3 receptor each caused receptor up- regulation but had markedly different functional effects on the cell.
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Hickstein, DD, RM Locksley, PG Beatty, A. Smith, DM Stone, and RK Root. "Monoclonal antibodies binding to the human neutrophil C3bi receptor have disparate functional effects." Blood 67, no. 4 (April 1, 1986): 1054–62. http://dx.doi.org/10.1182/blood.v67.4.1054.bloodjournal6741054.
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Three monoclonal antibodies (MAb)--OKMI, 7C3, and 60.3-- immunoprecipitated a common 170-kd neutrophil membrane antigen closely associated with, or identical to, the C3bi receptor (CR3). Despite binding to a common receptor, these antibodies displayed marked differences in their effects on C3bi-mediated neutrophil function as assessed by the binding and ingestion of opsonized zymosan and the subsequent triggering of the respiratory burst. Antibody 7C3 caused a time-dependent, irreversible inhibition of the neutrophil oxidative response to opsonized zymosan that correlated with capping of the bound antibody. In contrast, antibody 60.3 caused an immediate inhibition of the neutrophil oxidative response to opsonized zymosan that required the continuous presence of exogenous antibody to achieve the maximal inhibitory effect. Antibody OKMI demonstrated minimal inhibition of O2- release. Despite their functional differences, binding of either 7C3 or 60.3 led to up-regulation of new antigen, presumably from intracellular sites as previously described using OKMI. Crossed immunoprecipitations of radiolabeled neutrophil lysates indicated that each MAb bound to different antigens near or within the CR3 complex. Thus three MAb binding to the neutrophil CR3 receptor each caused receptor up- regulation but had markedly different functional effects on the cell.
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Brumbaugh, Gordon W., Lloyd E. Davis, John C. Thurmon, and Dwayne C. Savage. "Influence of Rhodococcus equi on the respiratory burst of resident alveolar macrophages from adult horses." American Journal of Veterinary Research 51, no. 5 (May 1, 1990): 766–71. http://dx.doi.org/10.2460/ajvr.1990.51.05.766.
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Summary Opsonized Rhodococcus equi activated the respiratory burst of resident alveolar macrophages (am) from adult horses in a logarithmic-linear, mass-related manner. The effect of R equi was not significantly different from that of equal masses of opsonized zymosan A. Therefore, R equi does not appear to attenuate the respiratory burst of equine am. The stimulatory effect of R equi was not reflected by increased production of superoxide anion (O2-), but increased activity of the hexose monophosphate shunt was observed. These results suggest a similarity between the respiratory burst of am from horses and that of am from rabbits. We concluded that resident am from adult horses do not produce O2- concurrently with an increase in activity of the hexose monophosphate shunt when stimulated with either opsonized zymosan A or opsonized R equi. This suggests that O2- is not an important component of the antibacterial defenses of equine am. Whether equine am are incapable of producing O2- or require different stimuli to produce it was not determined.
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Klebanoff, S. J., P. G. Beatty, R. D. Schreiber, H. D. Ochs, and A. M. Waltersdorph. "Effect of antibodies directed against complement receptors on phagocytosis by polymorphonuclear leukocytes: use of iodination as a convenient measure of phagocytosis." Journal of Immunology 134, no. 2 (February 1, 1985): 1153–59. http://dx.doi.org/10.4049/jimmunol.134.2.1153.
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Abstract Two monoclonal antibodies (Mab), designated 60.3 and 60.1, markedly inhibited the phagocytosis of serum-opsonized zymosan by human polymorphonuclear leukocytes (PMN) as measured by the iodination reaction and by microscopic visualization. These antibodies also inhibited rosette formation with EC3bi without decreasing EC3b rosetting, suggesting that Mab 60.3 and 60.1 inhibit the phagocytosis of opsonized zymosan through reaction with the C3bi receptor (CR3) on the leukocyte surface. In support of this concept is the finding that the PMN of two patients with recurrent infections do not ingest opsonized zymosan, lack C3bi receptor function, and react weakly or not at all with Mab 60.3 and 60.1. At concentrations which completely inhibited ingestion of opsonized zymosan, both Mab partially inhibited iodination with Staphylococcus aureus 502A as the particle, and did not affect iodination when Staphylococcus epidermidis was used. This presumably reflects a variable need among the opsonized particles for CR3 for ingestion. Mab 60.3 also inhibited the phagocytosis of certain unopsonized particles as measured by iodination, indicating that the antigens recognized by the Mab do not influence phagocytosis solely by functioning as a C3bi receptor. Mab 60.3 increased the phagocytosis of unopsonized, heat-killed S. aureus by reaction with the PMN via its antibody-combining site, and with the staphylococcal protein A via its Fc region (reverse opsonization). This process required protein A-containing organisms (S. aureus 502A or Cowan 1 but not S. aureus Wood 46 or S. epidermidis), was inhibited by purified protein A, and was not seen either when the F(ab')2 or Fab fragments of the antibody, or when PMN which lack or have low levels of the antigen were employed. Thus, these studies, using iodination as a convenient method for the measurement of phagocytosis, demonstrated two effects of antibodies directed against PMN cell surface components: inhibition of phagocytosis by reaction with the C3bi receptor, and stimulation of phagocytosis by reverse opsonization.
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Chan, Kin-Lun, Rena Bizios, and Asrar B. Malik. "Thrombin enhances opsonized zymosan-induced chemiluminescence of neutrophils." Tissue and Cell 20, no. 1 (January 1988): 13–17. http://dx.doi.org/10.1016/0040-8166(88)90003-1.
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Godfrey, RW, RM Manzi, MA Clark, and ST Hoffstein. "Stimulus-specific induction of phospholipid and arachidonic acid metabolism in human neutrophils." Journal of Cell Biology 104, no. 4 (April 1, 1987): 925–32. http://dx.doi.org/10.1083/jcb.104.4.925.
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Phospholipid remodeling resulting in arachidonic acid (AA) release and metabolism in human neutrophils stimulated by calcium ionophore A23187 has been extensively studied, while data obtained using physiologically relevant stimuli is limited. Opsonized zymosan and immune complexes induced stimulus-specific alterations in lipid metabolism that were different from those induced by A23187. [3H]AA release correlated with activation of phospholipase A2 (PLA2) but not with cellular activation as indicated by superoxide generation. The latter correlated more with calcium-dependent phospholipase C (PLC) activation and elevation of cellular diacylglycerol (DAG) levels. When cells that had been allowed to incorporate [3H]AA were stimulated with A23187, large amounts of labeled AA was released, most of which was metabolized to 5-HETE and leukotriene B4. Stimulation with immune complexes also resulted in the release of [3H]AA but this released radiolabeled AA was not metabolized. In contrast, stimulation with opsonized zymosan induced no detectable release of [3H]AA. Analysis of [3H]AA-labeled lipids in resting cells indicated that the greatest amount of label was incorporated into the phosphatidylinositol (PI) pool, followed closely by phosphatidylcholine and phosphatidylserine, while little [3H]AA was detected in the phosphatidylethanolamine pool. During stimulation with A23187, a significant decrease in labeled PI occurred and labeled free fatty acid in the pellet increased. With immune complexes, only a small decrease was seen in labeled PI while the free fatty acid in the pellets was unchanged. In contrast, opsonized zymosan decreased labeled PI, and increased labeled DAG. Phospholipase activity in homogenates from human neutrophils was also assayed. A23187 and immune complexes, but not zymosan, significantly enhanced PLA2 activity in the cell homogenates. On the other hand, PLC activity was enhanced by zymosan and immune complexes. Stimulated increases in PLC activity correlated with enhanced superoxide generation induced by the stimulus.
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Dyer, Robert M., Charles E. Benson, and Mary G. Boy. "Production of superoxide anion by bovine pulmonary macrophages challenged with soluble and particulate stimuli." American Journal of Veterinary Research 46, no. 2 (February 1, 1985): 336–41. https://doi.org/10.2460/ajvr.1985.46.02.336.
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SUMMARY The effects of opsonized zymosan, phorbal myristate acetate, and live Pasteurella haemolytica on superoxide anion production by bovine pulmonary macrophages were determined. The anion responses were dose-dependent for all stimuli, except for unopsonized P haemolytica. The effect of viable P haemolytica on macrophage viability was related to bacterial dosage and the presence of opsonizing antibody. Superoxide responses varied directly with the dose of opsonized live P haemolytica, but indirectly with macrophage viability.
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Bocca, Anamelia, Carolina Coelho, and Arturo Casadevall. "Dectin-1 pathway activation is important to Cryptococcus neoformans killing (67.10)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 67.10. http://dx.doi.org/10.4049/jimmunol.188.supp.67.10.
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Abstract Cryptococcus neoformans (Cn) is an encapsulated yeast that causes life-threatening meningoencephalitis in immunocompromised patients. The infectious propagules are inhaled into the host’s lug and interact with alveolar macrophages. An adequate pattern of macrophage activation is crucial to the outcome of the infection. However, it has been very difficult to demonstrate macrophage fungicidal activity in vitro. The main goal of this work was to determine if differential activation of macrophages by the dectin-1 pathway could increase Cn killing and improve host survival. Peritoneal macrophages were stimulated with zymozan and co-cultured ex vivo with opsonized Cn (H99) to allow phagocytosis. Our results showed that after zymozan stimulation of macrophages, fungal killing was increased. Stimulation with zymosan was more effective in fungal killing than stimulation with depleted-zymosan. Blockade of dectin-1 receptor reverted fungal killing to control levels only in macrophages stimulated with depleted zymozan. The ROS production was lower than in control groups. There was also a higher acidification of endosomes in zymozan-stimulated groups. Taken together, the data suggests that dectin-1 pathway activation by zymozan contributes to Cn killing. However, for the interaction between encapsulated C. neoformans cells and macrophages dectin-1 stimulation may be inadequate because the polysaccharide capsule blocks access to cell wall structures that trigger the dectin-1 receptor.
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Ushijima, Yoshio, Hiroko Totsune, Akira Nishida, and Minoru Nakano. "Chemiluminescence From Human Polymorphonuclear Leukocytes Activated With Opsonized Zymosan." Free Radical Biology and Medicine 22, no. 3 (January 1997): 401–9. http://dx.doi.org/10.1016/s0891-5849(96)00329-2.
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Chouinard, François C., Lynn Davis, Caroline Gilbert, and Sylvain G. Bourgoin. "Functional Role of AGAP2/PIKE-A in Fcγ Receptor-Mediated Phagocytosis." Cells 12, no. 1 (December 24, 2022): 72. http://dx.doi.org/10.3390/cells12010072.
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In phagocytes, cytoskeletal and membrane remodeling is finely regulated at the phagocytic cup. Various smaFll G proteins, including those of the Arf family, control these dynamic processes. Human neutrophils express AGAP2, an Arf GTPase activating protein (ArfGAP) that regulates endosomal trafficking and focal adhesion remodeling. We first examined the impact of AGAP2 on phagocytosis in CHO cells stably expressing the FcγRIIA receptor (CHO-IIA). In unstimulated CHO-IIA cells, AGAP2 only partially co-localized with cytoskeletal elements and intracellular compartments. In CHO-IIA cells, AGAP2 transiently accumulated at actin-rich phagocytic cups and increased Fcγ receptor-mediated phagocytosis. Enhanced phagocytosis was not dependent on the N-terminal GTP-binding protein-like (GLD) domain of AGAP2. AGAP2 deleted of its GTPase-activating protein (GAP) domain was not recruited to phagocytic cups and did not enhance the engulfment of IgG-opsonized beads. However, the GAP-deficient [R618K]AGAP2 transiently localized at the phagocytic cups and enhanced phagocytosis. In PLB-985 cells differentiated towards a neutrophil-like phenotype, silencing of AGAP2 reduced phagocytosis of opsonized zymosan. In human neutrophils, opsonized zymosan or monosodium urate crystals induced AGAP2 phosphorylation. The data indicate that particulate agonists induce AGAP2 phosphorylation in neutrophils. This study highlights the role of AGAP2 and its GAP domain but not GAP activity in FcγR-dependent uptake of opsonized particles.
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Pearson, R. D., P. Symes, M. Conboy, A. A. Weiss, and E. L. Hewlett. "Inhibition of monocyte oxidative responses by Bordetella pertussis adenylate cyclase toxin." Journal of Immunology 139, no. 8 (October 15, 1987): 2749–54. http://dx.doi.org/10.4049/jimmunol.139.8.2749.
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Abstract Bordetella pertussis and the other Bordetella species produce a novel adenylate cyclase toxin which enters target cells to catalyze the production of supraphysiologic levels of intracellular cyclic adenosine monophosphate (cAMP). In these studies, dialyzed extracts from B. pertussis containing the adenylate cyclase toxin, a partially purified preparation of adenylate cyclase toxin, and extracts from transposon Tn5 mutants of B. pertussis lacking the adenylate cyclase toxin, were used to assess the effects of adenylate cyclase toxin on human peripheral blood monocyte activities. Luminol-enhanced chemiluminescence of monocytes stimulated with opsonized zymosan was inhibited greater than 96% by exposure to adenylate cyclase toxin-containing extract, but not by extracts from adenylate cyclase toxin-deficient mutants. The chemiluminescence responses to particulate (opsonized zymosan, Leishmania donovani, and Staphylococcus aureus) and soluble (phorbol myristate acetate) stimuli were inhibited equivalently. The superoxide anion generation elicited by opsonized zymosan was inhibited 92% whereas that produced by phorbol myristate acetate was inhibited only 32% by B. pertussis extract. Inhibition of oxidative activity was associated with a greater than 500-fold increase in monocyte cAMP levels, but treated monocytes remained viable as assessed by their ability to exclude trypan blue and continued to ingest particulate stimuli. The major role of the adenylate cyclase toxin in the inhibition of monocyte oxidative responses was demonstrated by: 1) little or no inhibition by extracts from B. pertussis mutants lacking adenylate cyclase toxin; 2) high level inhibition with extract from B. parapertussis, a related species lacking pertussis toxin; and 3) a reciprocal relationship between monocyte cAMP levels and inhibition of opsonized zymosan-induced chemiluminescence using both crude extract and partially purified adenylate cyclase toxin. Pertussis toxin, which has been shown to inhibit phagocyte responses to some stimuli by a cAMP-independent mechanism, had only a small (less than 20%) inhibitory effect when added at concentrations up to 100-fold in excess of those present in B. pertussis extract. These data provide strong support for the hypothesis that B. pertussis adenylate cyclase toxin can increase cAMP levels in monocytes without compromising target cell viability or impairing ingestion of particles and that the resultant accumulated cAMP is responsible for the inhibition of oxidative responses to a variety of stimuli.
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Berger, F., U. Borchard, D. Hafner, and T. Weis. "Activation of a potassium outward current by zymosan and opsonized zymosan in mouse peritoneal macrophages." Naunyn-Schmiedeberg's Archives of Pharmacology 349, no. 6 (June 1994): 594–601. http://dx.doi.org/10.1007/bf01258465.
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Bussière, Françoise I., Elyett Gueux, Edmond Rock, Jean-Pierre Girardeau, Arlette Tridon, Andrzej Mazur, and Yves Rayssiguier. "Increased phagocytosis and production of reactive oxygen species by neutrophils during magnesium deficiency in rats and inhibition by high magnesium concentration." British Journal of Nutrition 87, no. 2 (February 2002): 107–13. http://dx.doi.org/10.1079/bjn2001498.
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Recent studies underline the importance of the immunoinflammatory processes in the pathology of Mg deficiency. Neutrophils possess a superoxide anion-generating NADPH oxidase and its inappropriate activation may result in tissue damage. The aim of the present study was to assess the effect of experimental Mg deficiency in the rat on polymorphonuclear leucocytes (PMN) activity and the role of increasing extracellular Mg. Weaning male Wistar rats were fed either a Mg-deficient or a control diet for 8 d. In Mg-deficient rats, the characteristic inflammatory response was accompanied by a marked increase in the number of PMN. Higher plasma interleukin 6 and NO concentrations and increased lipid peroxidation in the heart were found in Mg-deficient rats as compared with control rats. As shown by chemiluminescence studies, basal neutrophil activity from Mg-deficient rats was significantly elevated when compared with neutrophils from control rats. Moreover, the chemiluminescence of PMN from Mg-deficient rats was significantly higher than that of control rats following phorbol myristate acetate or opsonized zymosan activation. PMN from Mg-deficient rats also showed an increased activity of phagocytosis in comparison with neutrophils from control animals. Increasing extracellular Mg concentration in the incubating medium of PMN (0·8v.8·0 mM) decreased the chemiluminescence activity of PMN from control rats following opsonized zymosan activation. Chemiluminescence activities of PMN from Mg-deficient rats following phorbol myristate acetate or opsonized zymosan challenge were also decreased by high extracellular Mg concentration. From this work, it appears that PMN activation is an early consequence of Mg deficiency and that high extracellular Mg concentration inhibits free radicals generation.
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Etzioni, A., T. Meshulam, M. Zeltzer, A. Benderly, D. Merzbach, and P. Sujov. "Intralipid Effects on Preterm Neonate Serum." Journal of Pediatric Gastroenterology and Nutrition 6, no. 1 (January 1987): 105–8. http://dx.doi.org/10.1002/j.1536-4801.1987.tb09252.x.
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SummaryThe effects of Intralipid (IL) administration of preterm infants have been investigated. For this purpose, adult neutrophils were stimulated by infant sera collected before and after IL treatment. A definite decrease (p < 0.0005) in chemoattractant capacity of zymosan‐activated serum was observed after IL. On the other hand, no difference in the opsinizing abilities of untreated versus treated sera could be demonstrated by measuring the chemiluminescence responses to serum‐opsonized zymosan. This study emphasized the need of caution in the use of IL treatment for preterm infants.
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Zayasu, K., T. Fukushima, M. Yamaya, K. Sekizawa, K. Yamauchi, H. Sasaki, and T. Takishima. "Opsonized zymosan decreases cytoplasmic motility of alveolar macrophages in dogs." Respiration Physiology 89, no. 2 (August 1992): 249–60. http://dx.doi.org/10.1016/0034-5687(92)90054-z.
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Parnham, M. J., and C. Bittner. "Inhibition of macrophage chemiluminescence induced by PAF and opsonized zymosan." Prostaglandins 30, no. 4 (October 1985): 705. http://dx.doi.org/10.1016/0090-6980(85)90049-8.
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Heinle, Helmut, and Jasmin El Dessouki. "Luminol-enhanced chemiluminescence after reaction of hydroperoxides with opsonized zymosan." Journal of Bioluminescence and Chemiluminescence 10, no. 2 (March 1995): 71–76. http://dx.doi.org/10.1002/bio.1170100202.
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FOSTER, KEITH A., and KIM L. CRESCENZI. "A comparison of zymosan and opsonized zymosan as stimuli for arachidonic acid metabolism in human leucocytes." Biochemical Society Transactions 15, no. 3 (June 1, 1987): 417–18. http://dx.doi.org/10.1042/bst0150417.
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Tschakert, Jochen, and Wolfgang Voelter. "Festphasensynthese von Muramyldipeptidderivaten und Untersuchung ihrer biologischen Aktivität / Solid Phase Synthesis of Muramyl Dipeptide Derivatives and Investigations on their Biological Activities." Zeitschrift für Naturforschung B 49, no. 5 (May 1, 1994): 702–16. http://dx.doi.org/10.1515/znb-1994-0524.
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New muramyl dipeptide derivatives with exchanged carbohydrate residues are described. Each derivative is synthesized via a solid phase synthesis using an aminomethyl anchor resin. All synthetic products can be isolated in good yields. Their biological activities are tested by the luminol-dependent chemiluminescence associated with the phagocytosis of opsonized zymosan by granulocytes.
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Kurtasova, I. M., T. V. Lubnina, and E. V. Safontseva. "Сhanges in functional activity of peripheral blood neutrophils in young children with recurrent respiratory infection." Medical Immunology (Russia) 24, no. 2 (April 20, 2022): 407–12. http://dx.doi.org/10.15789/1563-0625-cif-2407.
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Neutrophils characterized by high mobility and ability for quick and accurate reresponse upon homeostatic changes. These changes primarily occur at the inflammation site. The pathogen elimination depends on the phagocytic activity of neutrophils. The data from past decades have revisited the role of neutrophils and their involvement in changing the human cellular and humoral immunity. Neutrophils are not only effector cells, but also regulatory cells of both innate and adaptive immunity. Our purpose was to study phagocytic activity and parameters of oxygen-dependent metabolism of peripheral blood neutrophils in young children with recurrent respiratory infections. We examined 111 children aged 1-3 years with recurrent respiratory infections over the period of clinical remission. The control group consisted of 24 healthy children aged 1-3 years. Phagocytic activity of peripheral blood neutrophils was studied by the latex test. Luminol-dependent chemiluminescence of blood neutrophils was studied according to de Sole et al. (1983). The study of phagocytic indexes of peripheral blood neutrophils in the children with recurrent respiratory infections has revealed a decrease in the number of actively phagocytizing cells and preservation of their absorptive capacity. Studies of luminol-dependent chemiluminescence in peripheral blood neutrophils in children with recurrent respiratory infections revealed changes in oxygen-dependent metabolism depending on the clinical variant of complicated infection. In the group of children with broncho-obstructive syndrome, the background chemiluminescence parameters of peripheral blood neutrophils were characterized by faster time to chemiluminescence curve peak. Chemiluminescence indices induced by opsonized zymosan showed a lower time of reaction to stimuli, decreased intensity of “respiratory burst”-associated luminescence, and decreased trend for activation index of peripheral blood neutrophils. Study of luminol-dependent chemiluminescence peripheral in blood neutrophils in children with hypertrophy of pharyngeal tonsils did not reveal changes in the background chemiluminescence levels. Chemiluminescence evaluation upon stimulation of peripheral blood neutrophils by opsonized zymosan caused a decrease in the stimulated response time, lower maximal “respiratory burst”, and decrease in AUC chemiluminescence. Thus, kinetics of spontaneous chemiluminescent response in peripheral blood neutrophils is impaired.in children with broncho-obstructive syndrome. Similarly, the in vitro neutrophil stimulation showed changes in chemiluminescent response kinetics and decreased reserve of oxygen-dependent metabolic capacity. In the children with hypertrophy of pharyngeal tonsil, we observed changes in chemiluminescent response of peripheral blood neutrophils only after opsonized zymosan induction. Compensatory metabolic capacity of peripheral blood neutrophils was retained in the opsonized zymosan stress tests. The study results showed unidirectional changes in peripheral blood neutrophil phagocytic activity parameters both in children with broncho-obstructive syndrome, and in children with pharyngeal tonsil hypertrophy and recurrent respiratory infection.
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Tapper, H., and S. Grinstein. "Fc receptor-triggered insertion of secretory granules into the plasma membrane of human neutrophils: selective retrieval during phagocytosis." Journal of Immunology 159, no. 1 (July 1, 1997): 409–18. http://dx.doi.org/10.4049/jimmunol.159.1.409.
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Abstract We studied the kinetics of secretion in human neutrophils stimulated by IgG-opsonized zymosan. Secretion of azurophilic and specific granules was quantified measuring the appearance of the granule markers CD63 and CD66b, respectively, at the cell surface. The kinetics of secretion was compared with the course of phagocytosis, revealed by the trapping of the fluid phase marker, Lucifer Yellow, in vacuoles containing zymosan particles. We found that secretion of both azurophilic and specific granules precedes phagosome sealing. An initial rapid phase of secretion was followed by a decrease in the amount of CD63 and CD66b at the cell surface. This subsequent disappearance of surface CD63 and CD66b was inhibited by cytochalasin B and probably represents internalization of the granular markers into the forming phagosome. The decrease in the amount of CD63 and CD66b exposed at the cell surface was not accompanied by a commensurate reduction in cell surface area, measured with the amphiphilic fluorescent dye FM1-43. These findings imply that CD63 and CD66b are selectively retrieved from the plasma membrane following secretion. Evidence is also presented that calcium is not the sole mediator of the rapid secretion of azurophilic and specific granules triggered by IgG-opsonized particles and that cytochalasin does not impair signaling of the calcium transient elicited by Fc receptors. Instead, actin disassembly appears to reduce the efficiency of the interaction between opsonized particles and their receptors, an effect that can be overcome by increasing the concentration of the stimulating particles.
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Kuo, Chih-Feng, Yee-Shin Lin, Woei-Jer Chuang, Jiunn-Jong Wu, and Nina Tsao. "Degradation of Complement 3 by Streptococcal Pyrogenic Exotoxin B Inhibits Complement Activation and Neutrophil Opsonophagocytosis." Infection and Immunity 76, no. 3 (January 3, 2008): 1163–69. http://dx.doi.org/10.1128/iai.01116-07.
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ABSTRACT Streptococcal pyrogenic exotoxin B (SPE B), a cysteine protease, is an important virulence factor in group A streptococcus (GAS) infection. The inhibition of phagocytic activity by SPE B may help prevent bacteria from being ingested. In this study, we examined the mechanism SPE B uses to enable bacteria to resist opsonophagocytosis. Using an enzyme-linked immunosorbent assay, we found that SPE B-treated serum impaired the activation of the classical, the lectin, and the alternative complement pathways. In contrast, C192S, a SPE B mutant lacking protease activity, had no effect on complement activation. Further study showed that cleavage of serum C3 by SPE B, but not C192S, blocked zymosan-induced production of reactive oxygen species in neutrophils as a result of decreased deposition of C3 fragments on the zymosan surface. Reconstitution of C3 into SPE B-treated serum unblocked zymosan-mediated neutrophil activation dose dependently. SPE B-treated, but not C192S-treated, serum also impaired opsonization of C3 fragments on the surface of GAS strain A20. Moreover, the amount of C3 fragments on the A20 cell surface, a SPE B-producing strain, was less than that on its isogenic mutant strain, SW507, after opsonization with normal serum. A20 opsonized with SPE B-treated serum was more resistant to neutrophil killing than A20 opsonized with normal serum, and SPE B-mediated resistance was C3 dependent. These results suggest a novel SPE B mechanism, one which degrades serum C3 and enables GAS to resist complement damage and opsonophagocytosis.
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Yazdanbakhsh, M., C. M. Eckmann, and D. Roos. "Characterization of the interaction of human eosinophils and neutrophils with opsonized particles." Journal of Immunology 135, no. 2 (August 1, 1985): 1378–84. http://dx.doi.org/10.4049/jimmunol.135.2.1378.
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Abstract The interaction of human eosinophils with opsonized particles was compared with that of human neutrophils. When eosinophils are stimulated with serum-opsonized zymosan particles, the lag time in H2O2 production is twice as long as found with neutrophils. Moreover, the concentration of these IgG + C3-coated particles required for optimal stimulation is about four times as high for eosinophils as for neutrophils. Under these conditions, the two cell types generate similar amounts of H2O2. However, eosinophils produce twice as much H2O2 as do neutrophils when stimulated with the soluble agent phorbol myristate acetate. Thus, although the oxidase capacity of eosinophils is larger than that of neutrophils, opsonized zymosan is a weak trigger for this activity in eosinophils. This phenomenon may be due to differences between the two cell types in the plasma membrane receptors or in the receptor oxidase transducing signal. The following are indications for the first possibility. i) IgG interacts poorly with the Fc gamma receptors on the eosinophil surface compared with those on neutrophils. This was shown by the inability of IgG-coated zymosan or IgG-coated latex to trigger any substantial H2O2 production by eosinophils unless brought into close contact with these cells by centrifugation. In contrast, neutrophils are stimulated by these particles both in suspension and in a pellet. The dissimilarity of the Fc gamma receptors on eosinophils and neutrophils was also shown with respect to antigenicity, determined by the monoclonal antibodies 3G8 and CLB-FcR-1. ii) Eosinophils contain about half as many receptors for C3b and C3bi on their surface as do neutrophils, also detected with monoclonal antibodies. The interaction of IgG subclasses with functional Fc gamma receptors on eosinophils and neutrophils showed that eosinophils release twice as much H2O2 as do neutrophils upon interaction with IgG1-, IgG2-, or IgG3-coated Sepharose beads, but this difference becomes fivefold with IgG4-coated Sepharose. This might be of relevance to the situation of chronic antigenic stimulation, e.g., in chronic schistosomiasis, in which eosinophil numbers and IgG4 antibody levels are elevated.
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Bruynzeel, Pieter L. B., Paul T. M. Kok, Maartje L. Hamelink, Arda M. Kijne, and Jan Verhagen. "Exclusive leukotriene C4synthesis by purified human eosinophils induced by opsonized zymosan." FEBS Letters 189, no. 2 (September 23, 1985): 350–54. http://dx.doi.org/10.1016/0014-5793(85)81054-1.
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Leino, Lasse, Helena Tuominen, Kirsi Lehtola, Karl E. O. Åkerman, and Kari Punnonen. "Biphasic formation of inositol phosphates in opsonized zymosan-stimulated human neutrophils." Cellular Signalling 7, no. 4 (May 1995): 397–402. http://dx.doi.org/10.1016/0898-6568(94)00094-r.
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Malik, Zulfiqar A., Gerene M. Denning, and David J. Kusner. "Inhibition of Ca2+ Signaling by Mycobacterium tuberculosisIs Associated with Reduced Phagosome–Lysosome Fusion and Increased Survival within Human Macrophages." Journal of Experimental Medicine 191, no. 2 (January 17, 2000): 287–302. http://dx.doi.org/10.1084/jem.191.2.287.
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Complement receptor (CR)-mediated phagocytosis of Mycobacterium tuberculosis by macrophages results in intracellular survival, suggesting that M. tuberculosis interferes with macrophage microbicidal mechanisms. As increases in cytosolic Ca2+ concentration ([Ca2+]c) promote phagocyte antimicrobial responses, we hypothesized that CR phagocytosis of M. tuberculosis is accompanied by altered Ca2+ signaling. Whereas the control complement (C)-opsonized particle zymosan (COZ) induced a 4.6-fold increase in [Ca2+]c in human macrophages, no change in [Ca2+]c occurred upon addition of live, C-opsonized virulent M. tuberculosis. Viability of M. tuberculosis and ingestion via CRs was required for infection of macrophages in the absence of increased [Ca2+]c, as killed M. tuberculosis or antibody (Ab)-opsonized, live M. tuberculosis induced elevations in [Ca2+]c similar to COZ. Increased [Ca2+]c induced by Ab-opsonized bacilli was associated with a 76% reduction in intracellular survival, compared with C-opsonized M. tuberculosis. Similarly, reversible elevation of macrophage [Ca2+]c with the ionophore A23187 reduced intracellular viability by 50%. Ionophore-mediated elevation of [Ca2+]c promoted the maturation of phagosomes containing live C-opsonized bacilli, as evidenced by acidification and accumulation of lysosomal protein markers. These data demonstrate that M. tuberculosis inhibits CR-mediated Ca2+ signaling and indicate that this alteration of macrophage activation contributes to inhibition of phagosome–lysosome fusion and promotion of intracellular mycobacterial survival.
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Labro, M. T., J. el Benna, N. Charlier, H. Abdelghaffar, and J. Hakim. "Cefdinir (CI-983), a new oral amino-2-thiazolyl cephalosporin, inhibits human neutrophil myeloperoxidase in the extracellular medium but not the phagolysosome." Journal of Immunology 152, no. 5 (March 1, 1994): 2447–55. http://dx.doi.org/10.4049/jimmunol.152.5.2447.
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Abstract Cefdinir, a new oral 2-amino-5-thiazolyl cephalosporin, inhibited the luminol-amplified chemiluminescence (LACL) response of human neutrophils stimulated by PMA but not opsonized zymosan, in a concentration-dependent but not time-dependent manner. The LACL response to opsonized zymosan in cytochalasin B-treated neutrophils was, however, inhibited by cefdinir. Various cephalosporins, regardless of the presence of a 2-amino-5-thiazolyl moiety, did not significantly alter the neutrophil LACL response triggered by PMA and zymosan. The LACL response induced by the calcium ionophore A23187 and FMLP was also impaired by cefdinir, and this impairment was increased in cytochalasin B-treated neutrophils. Superoxide anion generation by neutrophils, measured in terms of lucigenin-amplified chemiluminescence and cytochrome c reduction, was not altered. Spontaneous and FMLP-induced neutrophil degranulation, assessed by lysozyme and beta-glucuronidase release, were not modified by cefdinir. Furthermore, cefdinir inhibited LACL generation in cell-free systems consisting of H2O2, NaI, and either horseradish peroxidase or a myeloperoxidase-containing neutrophil extract. Orthodianisidine oxidation in these two acellular systems was inhibited by cefdinir. Cefdinir did not alter neutrophil bacterial killing at concentrations that inhibited myeloperoxidase-containing neutrophil extract-dependent reactions induced by soluble stimuli. Taken together, these data strongly suggest that cefdinir directly inhibits the activity of myeloperoxidase-containing neutrophil extract released into the extracellular medium during neutrophil stimulation by soluble mediators, but has no effect on that released into the phagolysosome during phagocytosis. This unusual property of a member of the beta-lactam family could be of interest in modulating the exaggerated inflammatory process often associated with infectious diseases.
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van der Bruggen, T., P. T. Kok, J. A. Raaijmakers, J. W. Lammers, and L. Koenderman. "Cooperation between Fc gamma receptor II and complement receptor type 3 during activation of platelet-activating factor release by cytokine-primed human eosinophils." Journal of Immunology 153, no. 6 (September 15, 1994): 2729–35. http://dx.doi.org/10.4049/jimmunol.153.6.2729.
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Abstract After priming with cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-3, or IL-5, eosinophils are stimulated potently by opsonized particles like serum-treated zymosan (STZ), resulting in activation of the respiratory burst and production of lipid mediators, such as platelet-activating factor (PAF) and leukotriene C4 (LTC4). In the present study, the role of the opsonin receptors Fc gamma RII and CR3 during both STZ-induced activation of the respiratory burst and PAF release by human eosinophils was investigated. Inhibition studies with blocking mAbs (alpha hFc gamma RII: AT10, IV.3; alpha CR3: B2.12, 44a) showed that both Fc gamma RII and CR3 are important for STZ-induced PAF release by cytokine-primed eosinophils. In contrast, CR3 is involved in activation of the respiratory burst, whereas Fc gamma RII seems not to be important, because blocking anti-Fc gamma RII mAbs had no effect. Subsequently, experiments were performed with zymosan particles coated with IgG, iC3b, or a combination of both. IgG-coated particles poorly activated both responses in GM-CSF primed and unprimed cells. iC3b-Zymosan activated the respiratory burst as well as zymosan expressing both opsonins (IgG/iC3b-zymosan). In contrast, iC3b-zymosan induced significantly less PAF release by GM-CSF-primed eosinophils than did IgG/iC3b-zymosan, suggesting synergism between Fc gamma RII and CR3. This synergistic effect was not observed when IgG-zymosan and iC3b-zymosan were added simultaneously. Therefore, these data indicate that on human eosinophils, Fc gamma RII and CR3 act synergistically to activate PAF release, provided that their ligands are in close proximity.
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Watson, G. L., R. F. Slocombe, N. E. Robinson, and S. D. Sleight. "Definition of chemiluminescence and superoxide production responses of bovine neutrophils to selected soluble and particulate stimulants, and comparisons with the responses to Pasteurella haemolytica." American Journal of Veterinary Research 56, no. 8 (August 1, 1995): 1045–54. http://dx.doi.org/10.2460/ajvr.1995.56.08.1045.
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SUMMARY We defined methods for use of luminol-dependent chemiluminescence (ldcl) and superoxide anion (O2-) production as parameters of the oxidative metabolism of neutrophils isolated from 1.5- to 5-week-old neonatal calves. We determined how variations in blood sample handling, agonist preparation, individual variability, and age of calves influenced the ldcl and O2- responses to certain agonists, and defined concentrations of soluble and particulate agonists that maximally stimulated the oxidative metabolism of bovine neutrophils. Oxidative responses, particularly ldcl, were characterized by marked day-to-day variability, differed greatly within and between calves, were partially age-dependent, and were partially dependent on the individual agonist. Superoxide anion production had substantially less variability. We compared the in vitro oxidative (ldcl and O2-) responses of neutrophils isolated from neonatal calves stimulated by defined concentrations of the agonists–latex, phorbol myristate acetate, calcium ionophore, and opsonized zymosan–with responses to formylated oligopeptides and zymosan-activated serum, and to live, dead, live opsonized, and dead opsonized Pasteurella haemolytica organisms. Opsonization of particulates, pathogenic or nonpathogenic, enhanced the ldcl and O2- responses of stimulated neutrophils although P haemolytica was a less potent stimulant of oxidative functions than were nonbiological agonists. We conclude that the generation of reactive oxygen species by bovine neutrophils in response to P haemolytica is highly dependent on the presence of opsonins and is greatly enhanced in live vs killed bacteria. Furthermore, the in vitro generation of reactive oxygen species, including O2- by stimulated neutrophils, may be of biologic importance if similar events occur in vivo, and could have a major role in the pathogenesis of the acute lung injury associated with pneumonic pasteurellosis.
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Cassone, M. C. "Effects of 2-arylpropionic acids on chemiluminescence during phagocytosis of opsonized zymosan." Pharmacological Research Communications 20 (September 1988): 81. http://dx.doi.org/10.1016/s0031-6989(88)80211-x.
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Ishitani, K., A. Matsuura, and H. Honda. "Auranofin inhibits calcium uptake into opsonized-zymosan-stimulated neutrophils obtained from rats." Inflammation Research 44, no. 11 (November 1995): 482–85. http://dx.doi.org/10.1007/bf01837914.
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Xia, Yu, Václav Větvička, Jun Yan, Margareta Hanikýřová, Tanya Mayadas, and Gordon D. Ross. "The β-Glucan-Binding Lectin Site of Mouse CR3 (CD11b/CD18) and Its Function in Generating a Primed State of the Receptor That Mediates Cytotoxic Activation in Response to iC3b-Opsonized Target Cells." Journal of Immunology 162, no. 4 (February 15, 1999): 2281–90. http://dx.doi.org/10.4049/jimmunol.162.4.2281.
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Abstract Mouse leukocyte CR3 (Mac-1, αMβ2 integrin) was shown to function as a receptor for β-glucans in the same way as human CR3. Soluble zymosan polysaccharide (SZP) or pure β-glucans labeled with FITC or 125I bound in a saturable and reversible manner to neutrophils, macrophages, and NK cells. This lectin activity was blocked by anti-CD11b mAb M1/70 or 5C6 and did not occur with leukocytes from CR3−/− (CD11b-deficient) mice. SZP preparations containing primarily mannose or glucose bound to CR3, and the binding of 125I-labeled β-glucan to CR3 was competitively inhibited by β-glucans from barley or seaweed, but not by yeast α-mannan. Also, as with human CR3, the lectin site of mouse CR3 was inhibited by α- or β-methylglucoside (but not d-glucose), α- or β-methylmannoside, and N-acetyl-d-glucosamine. Phagocytosis of zymosan and serum-opsonized zymosan was partially inhibited by anti-CR3 and was reduced to <40% of normal with leukocytes from CR3−/− mice. As with neutrophils from patients with CD18 deficiency, neutrophils from CR3−/− mice exhibited no phagocytosis of particulate β-glucan. SZP or β-glucans primed CR3 of neutrophils, macrophages, and NK cells for cytotoxicity of iC3b-opsonized tumor cells that otherwise did not trigger killing. β-Glucan priming for cytotoxicity was inhibited by anti-CR3 and did not occur with leukocytes from CR3−/− mice. The primed state of macrophage and NK cell CR3 remained detectable for 18 to 24 h after pulsing with β-glucans. The similarity of mouse and human CR3 in response to β-glucans highlights the utility of mouse tumor models for development of therapeutic β-glucans.
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Di Carlo, Andrea L., Max J. Paape, and Robert H. Miller. "Reactivity of purified complement component 3b with bovine neutrophils and modulation of complement receptor 1." American Journal of Veterinary Research 57, no. 2 (February 1, 1996): 151–56. http://dx.doi.org/10.2460/ajvr.1996.57.02.151.
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Abstract Objective To study binding of purified complement component C3b to bovine blood and mammary neutrophils (PMN) after various treatments and determine their ability to modulate receptor numbers. Design Cell isolation, activation, and flow cytometric studies. Animals Healthy lactating Holstein cattle. Procedure Complement component C3b (18,300 kd) was isolated from bovine serum by column chromatography, and flow cytometric assays using fluorescein isothiocyanate-labeled C3b were developed to evaluate binding to PMN complement receptor 1. Multiple substances were tested to determine their overall effect on C3b binding to PMN. Blood and milk PMN were isolated by differential centrifugation and exposed to optimal concentrations of recombinant human C5a, formyl-methyl leucyl phenylalanine, recombinant bovine interferon-γ, variable concentrations of phorbol myristate acetate (0.01 to 100 ng), calcium ionophore A23187, serum-opsonized zymosan, zymosan-activated serum (ZAS), zymosan-activated plasma (ZAP), and hydrocortisone acetate (25 and 70 ng). Additionally, mammary and blood PMN were preincubated in skim milk and whey. Results Variable concentrations of phorbol myristate acetate caused a dose-dependent increase in percentage of PMN binding C3b, and increased the amount of C3b bound per cell. Significant increases were observed after PMN treatment with calcium ionophore, serum opsonized zymosan, ZAS, and ZAP; conversely, incubation of PMN with hydrocortisone acetate resulted in reduced overall binding of C3b. Mammary PMN consistently bound more C3b, which was attributed to their activation during migration into the mammary gland. Binding of C3b was inhibited by skim milk. Activation of blood PMN with PMA, ZAS, and ZAP elicited larger responses than those observed for mammary PMN. Conclusions Modulation of complement receptors on bovine PMN is possible. Additionally, significant difference between the level of binding of C3b to blood and milk PMN, with milk PMN having higher binding, may be attributable to migration of PMN into the mammary gland, causing increased receptor expression. Clinical Relevance Contribution to a greater understanding of the role of complement in bovine immunologic systems, leading to testing for in vivo enhancement of bovine immune responses to invading pathogens.
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Smirnova, O. V., E. V. Kasparov, Ya I. Perepechay, A. A. Nesytykh, and V. S. Belyaev. "FEATURES OF NEUTROPHIL CHEMILUMINESCENCE IN THE PATIENTS WITH ADVANCED RECTAL CANCER." Medical Immunology (Russia) 21, no. 1 (January 24, 2019): 157–64. http://dx.doi.org/10.15789/1563-0625-2019-1-157-164.
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Colorectal cancer is one of the most common malignant diseases in Russia worldwide making up 5-6% of all human malignant tumors. Neutrophilic granulocytes are actively involved in development of antitumor response. A key role in tumor regression is assigned to active forms of oxygen produced by neutrophils. In connection with these pre-requisites, our goal was to study functional characteristics of spontaneous and induced chemiluminescent activity of neutrophil granulocytes in patients with rectal cancer before starting pathogenetic therapy and in subsequent dynamics. The paper presents some laboratory results, i.e., functional indices of neutrophilic granulocytes’ activity in 36 patients with rectal cancer being at different stages of oncological process. The control group consisted of 112 practically healthy volunteers, comparable in sex and age to the group of patients under study. To perform the study venous blood was taken from patients to vacuum test tubes with lithium heparin in the morning time before surgical treatment, and on day 7 after the surgical intervention. Evaluation of spontaneous and induced chemiluminescence was performed for 90 minutes in a 36-channel “CL 3606” chemiluminescence analyzer (Russia). The following characteristics were determined: time of the curve transition to maximal chemiluminescence intensity (Tmax), maximal value of chemiluminescence intensity (Imax), integral area under the chemiluminescence curve (S). Luminol was used as the chemiluminescence enhancer. Opsonized zymosan was used to induce the respiratory explosion. Chemiluminescence amplification induced by opsonized zymosan was evaluated by the ratio of induced-tospontaneous chemiluminescence (Sind/spont) designated as an activation index.Analysis of chemiluminescence activity in neutrophilic granulocytes showed a significant increase in spontaneous chemiluminescence activity at the stages III and IV of the disease. The production of active oxygen forms induced in neutrophilic granulocytes by opsonized zymosan increased in all the study groups, relative to control parameters. The area under the curves of spontaneous and induced chemiluminescence in patients with colorectal cancer at all stages of the oncological process is less, as compared to the control group, which, despite high indices of maximal chemiluminescence activity, may indicate insufficient total production of reactive oxygen species. The time-to-peak values of the chemiluminescence curves in patients with rectal cancer at all stages of the disease did not show statistically significant differences from the control group.
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Pascual, A., I. García, S. Ballesta, and E. J. Perea. "Uptake and intracellular activity of trovafloxacin in human phagocytes and tissue-cultured epithelial cells." Antimicrobial Agents and Chemotherapy 41, no. 2 (February 1997): 274–77. http://dx.doi.org/10.1128/aac.41.2.274.
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The penetration of trovafloxacin into human polymorphonuclear leukocytes (PMNs), human peritoneal macrophages, and tissue-cultured epithelial cells (McCoy cells) was evaluated. The cellular concentration to extracellular concentration (C/E) ratios of trovafloxacin were greater than 9 for extracellular concentrations ranging from 0.5 to 25 micrograms/ml. The uptake of trovafloxacin by PMNs was rapid, reversible, nonsaturable, not energy dependent, and significantly increased at 4 degrees C. Ingestion of opsonized zymosan, but not opsonized Staphylococcus aureus, significantly increased the amount of PMN-associated trovafloxacin. This agent at concentrations of 0.5 and 1 microgram/ml induced a greater reduction in the survival of intracellular S. aureus in PMNs than ciprofloxacin and ofloxacin. It was concluded that trovafloxacin reaches concentrations within phagocytic and nonphagocytic cells several times higher than the extracellular ones, while it remains active in PMNs.
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Schultz, R. M., S. K. Nanda, and M. G. Altom. "Effects of various inhibitors of arachidonic acid oxygenation on macrophage superoxide release and tumoricidal activity." Journal of Immunology 135, no. 3 (September 1, 1985): 2040–44. http://dx.doi.org/10.4049/jimmunol.135.3.2040.
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Abstract Macrophages release a variety of arachidonic acid metabolites after treatment with various membrane triggers or particulate stimuli. We examined the role of phospholipase and lipoxygenase inhibitors in the modulation of superoxide production and tumor cytolysis by murine macrophages. Superoxide was induced by the soluble stimulus, phorbol myristate acetate (PMA), and the particulate stimulus, opsonized zymosan, and was measured by the reduction of ferricytochrome c with the use of a micro ELISA reader. Macrophage-mediated tumor cytolysis was induced by hybridoma-derived, macrophage-activating factor (MAF) and was quantitated by 51Cr release from P815 target cells. In both assays, 72-hr peptone-elicited macrophages were used. Dexamethasone, and to a lesser degree hydrocortisone, inhibited superoxide release and MAF-induced tumor cytolysis. Inhibition in the superoxide assay required pretreatment with corticosteroid. Only the gold compound, auranofin, inhibited superoxide when given simultaneously with stimulant. Other phospholipase inhibitors, including mepacrine and 4-bromophenacyl bromide, and several lipoxygenase inhibitors, including BW755c, nordihydroguaiaretic acid (NDGA), and 5,8,11,14-eicosatetraynoic acid (ETYA), failed to modulate either macrophage response at nontoxic concentrations. At the concentrations tested in the tumoricidal and superoxide assays, mepacrine and 4-bromophenacyl bromide inhibited the release of 14C-arachidonic acid from macrophages stimulated with opsonized zymosan. Our data strongly suggest that corticosteroids suppress macrophage superoxide production and tumoricidal function by a nonphospholipase-dependent mechanism.
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Gil-de-Gómez, Luis, Patricia Monge, Juan P. Rodríguez, Alma M. Astudillo, María A. Balboa, and Jesús Balsinde. "Phospholipid Arachidonic Acid Remodeling During Phagocytosis in Mouse Peritoneal Macrophages." Biomedicines 8, no. 8 (August 5, 2020): 274. http://dx.doi.org/10.3390/biomedicines8080274.
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Macrophages contain large amounts of arachidonic acid (AA), which distributes differentially across membrane phospholipids. This is largely due to the action of coenzyme A-independent transacylase (CoA-IT), which transfers the AA primarily from diacyl choline-containing phospholipids to ethanolamine-containing phospholipids. In this work we have comparatively analyzed glycerophospholipid changes leading to AA mobilization in mouse peritoneal macrophages responding to either zymosan or serum-opsonized zymosan (OpZ). These two phagocytic stimuli promote the cytosolic phospholipase A2-dependent mobilization of AA by activating distinct surface receptors. Application of mass spectrometry-based lipid profiling to identify changes in AA-containing phospholipids during macrophage exposure to both stimuli revealed significant decreases in the levels of all major choline phospholipid molecular species and a major phosphatidylinositol species. Importantly, while no changes in ethanolamine phospholipid species were detected on stimulation with zymosan, significant decreases in these species were observed when OpZ was used. Analyses of CoA-IT-mediated AA remodeling revealed that the process occurred faster in the zymosan-stimulated cells compared with OpZ-stimulated cells. Pharmacological inhibition of CoA-IT strongly blunted AA release in response to zymosan but had only a moderate effect on the OpZ-mediated response. These results suggest a hitherto undescribed receptor-dependent role for CoA-independent AA remodeling reactions in modulating the eicosanoid biosynthetic response of macrophages. Our data help define novel targets within the AA remodeling pathway with potential use to control lipid mediator formation
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Matsui, Sachiko, Sachiko Matsumoto, Reiko Adachi, Kaoru Kusui, Akiko Hirayama, Hidemi Watanabe, Kazumasa Ohashi, et al. "LIM Kinase 1 Modulates Opsonized Zymosan-triggered Activation of Macrophage-like U937 Cells." Journal of Biological Chemistry 277, no. 1 (November 2, 2001): 544–49. http://dx.doi.org/10.1074/jbc.m110153200.
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Lum, Hazel, Lester Gibbs, Linda Lai, and Asrar B. Malik. "CD18 integrin-dependent endothelial injury: effects of opsonized zymosan and phorbol ester activation." Journal of Leukocyte Biology 55, no. 1 (January 1994): 58–63. http://dx.doi.org/10.1002/jlb.55.1.58.
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