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At least 973 records · Page 54Linked to original sources
PubMed1988

Stimulation of eosinophil adherence to human vascular endothelial cells in vitro by platelet-activating factor.

111In-Labeled eosinophils from mildly eosinophilic subjects have been examined for their capacity to adhere to cultured human umbilical vein endothelial cells. In assay buffer alone, 32.0% +/- 2.6 eosinophils adhered spontaneously to endothelial cells. Platelet-activating factor (PAF) (1-alkyl-2-acetyl-sn-glycero-3-phosphorylcholine) at concentrations as low as 10(-9) M increased this adherence to a level of 46.7% +/- 2.0. The effects of PAF were confirmed to be on eosinophils by parallel adherence assays done on serum-coated plastic plates where comparably enhanced adhesion of the eosinophils was seen. Lyso-PAF, the biologically inactive precursor/metabolite of PAF, had no stimulatory properties. FMLP caused an increase in eosinophil adherence, comparable to that of PAF, but only at high concentrations (10(-6) to 10(-7) M). Further examination of eosinophil subpopulations separated on metrizamide gradients indicated that "hypodense" eosinophils had a significantly higher ability to adhere spontaneously to endothelial cells than "normal" dense eosinophils, (35.5% +/- 4.2 vs 23.8% +/- 2.5, respectively) and could be stimulated with PAF to higher levels, although the magnitude of stimulation was similar for both populations. A mouse mAb TS1/18 to the common beta-subunit of the Mac-1 cell surface glycoprotein complex (CDw18) reduced by up to 94.6% the PAF-induced increase in adherence, but had no effect on the spontaneous adhesion. Eosinophils were also shown by cytofluorography to be capable of binding the TS1/18 antibody on their cell surface, and in some experiments to exhibit an increased expression of the Mac-1 complex on stimulation with PAF. These studies indicate that eosinophils are capable of binding to endothelial cells in culture, that PAF is a potent stimulator of eosinophil adherence, and that the Mac-1 complex has a critical role in this adhesion process.

Antibodies, Monoclonal↗
PubMed1986

Binding of immunoglobulin classes and subclasses to human neutrophils and eosinophils.

A comparative study of membrane expression of immunoglobin (Fc) receptors on human eosinophils and neutrophils has been undertaken using human IgG-1, IgG-2, IgG-3, IgG-4, IgA-1, IgA-2, IgM, IgD and IgE myeloma proteins. Sheep erythrocytes (E) coated with either human IgG-1, IgG-2, IgG-3 or IgG-4 myeloma proteins formed rosettes with human neutrophils and eosinophils. Proportionally more (1 1/2-2 times) rosettes were observed with neutrophils compared to eosinophils. In contrast, E-IgE bound to eosinophils (but not to neutrophils) to a degree that was comparable to E-IgG-1. Although IgG and IgE rosettes were inhibited by aggregates prepared from their corresponding myeloma protein there was no evidence that eosinophils and neutrophils have distinct receptors for IgG subclasses. Cells from four patients with hypereosinophilia were separated on density (metrizamide) gradients. The percentages of E-IgG-1 and E-IgE rosettes with normal- and light-density eosinophils were similar. Neutrophils, but not eosinophils, also bound significantly more E-IgA-1 and E-IgA-2 than the E-human albumin (E-Alb) control. In contrast, neutrophil and eosinophil rosette formation with E-IgM and E-IgD was not significantly different from E-Alb or E alone. These experiments indicate that human neutrophils and eosinophils bind homologous IgG subclass myeloma proteins, eosinophils, but not neutrophils, bind E-IgE with a similar avidity to that observed with E-IgG1, neutrophils, but not eosinophils, readily express demonstrable receptors for IgA-1 and IgA-2 and neither neutrophils nor eosinophils form E-IgM or E-IgD rosettes in greater numbers than the E-Alb controls.

Dose-Response Relationship, Immunologic↗
PubMed1983

In vitro interaction of eosinophils from ascarid-infected eyes with Ascaris suum and Toxocara canis larvae.

The role of eosinophils in ocular ascarid infection is studied in an animal model. Primary intravitreal infection of guinea-pig eyes with ascarid (Toxocara canis, Ascaris suum) second-stage (L2) larvae resulted in an anterior chamber exudate containing 98% or more eosinophils. Anterior chamber aspirates were cultured in RPMI media 1640 with T. canis or A. suum L2 larvae at 37 degrees C for 1-96 hours. The in vitro interaction of eosinophils with L2 larvae was studied by light, and scanning and transmission electron microscopy. Eosinophil interaction with L2 larvae in vitro was dependent upon soluble factors present in the anterior chamber aspirates from the infected eyes. Eosinophils adhered firmly to the surface of the L2 larvae, to a larval sheath, or to attached eosinophils. Eosinophils interacting with larvae displayed a range of granular matrix changes, core duplication, and reversal of the relative electron densities of the core and matrix, suggestive of eosinophil activation. An eosinophil secretory granule was seen to empty its contents onto a T. canis L2 larval surface. Electron-dense material was observed in the interphase between eosinophils and the larval cuticle or sheath. Large lipid droplets within muscle cells and ballooned-out epidermal cells were seen within larvae immediately beneath adherent eosinophils. Parasites were able to partially evade interaction with eosinophils in culture by shedding their sheaths. A similar phenomenon in vivo may allow the parasite to migrate from a site of inflammation. It is possible that a discarded sheath or membrane serves as an antigenic stimulus for a local intraocular granulomatous reaction free of parasite.

Animals↗
PubMed1994

[Inhibitory effect of TGF-beta 1 on cytokine-enhanced eosinophil survival].

TGF-beta 1 has many biological activities in various cell types and is regarded as a multifunctioning regulator of cell growth. We studied the effect of TGF-beta 1 on cytokine-enhanced eosinophil survival in vitro. Eosinophils were purified from patients with mild atopic dermatitis by Percoll density gradient centrifugation and the CD16 negative selection/immunomagnetic beads technique. Eosinophil purity was greater than 95%. The purified eosinophils were incubated in the presence of eosinophil-activating cytokines (IL-5, IL-3, GM-CSF, IFN-gamma) with and without TGF-beta 1 for 3 days. Eosinophil viability was determined by staining the cells with fluorescein diacetate and propidium iodide. Without cytokine, most eosinophils died by day 3 in culture, but human recombinant IL-5, IL-3, GM-CSF, and IFN-gamma enhanced eosinophil survival in a dose-dependent manner. To test the effect of TGF-beta 1 on enhanced eosinophil survival, eosinophils were cultured with activating cytokine and TGF-beta 1. TGF-beta 1 inhibited eosinophil survival in a dose-dependent manner. The inhibitory effects of TGF-beta 1 on IL-5 enhanced survival was partially reversed by high concentrations of IL-5 and was completely neutralized with anti-TGF-beta antibody. Moreover, the apoptosis of eosinophils induced by TGF-beta 1 was determined with the assay of DNA fragmentation on agarose gel electrophoresis. It is possible that TGF-beta 1 activates the pathway of apoptosis. The results suggest that TGF-beta 1 may play a crucial role in the regulation of allergic inflammation.

Apoptosis↗
PubMed1994

[The immunologic role of eosinophilic granulocytes within the scope of inflammatory lung diseases].

Although identified over a hundred years ago, the precise role of the eosinophil in eosinophil-associated diseases still remains undefined. However, the results of modern cellular, immunological, and biochemical investigations have suggested that eosinophils contain unique constituents and functional adaptions through which eosinophils gain a profound cytotoxic capacity. This property may not only be crucial for the host defence mechanism against helminthic infections but may also be involved in the pathogenesis of chronic inflammation associated with allergic reaction and other eosinophilic disorders. There is increasing evidence available that the eosinophil may cause damage to host tissue and elicit tissue fibrosis. The eosinophil appears to adapt certain general cellular characteristics during its ontogeny and participation in inflammatory reactions, such as hypodensity, expression and induction of surface markers and adhesion molecules. In addition, there is evidence that the eosinophil may undergo a shift between hypo- and hyperreactivity states. Factors regulating the level of eosinophil activation may include both lipid mediators and cytokines released by macrophages, mast cells, platelets, endothelial cells, and T lymphocytes. The rapidly evolving understanding of the functional properties of the eosinophil will further help to define the pathogenesis of certain eosinophilic disorders and may provide the basis for new therapeutic strategies in eosinophilic disorders.

Cytotoxicity, Immunologic↗
PubMed1993

Activated eosinophils evoke chloride secretion in model intestinal epithelia primarily via regulated release of 5'-AMP.

Eosinophils may be prominent in intestinal diseases including allergic gastroenteritis, inflammatory bowel disease, enteritis associated with hypereosinophilic syndromes (HES), and parasitic diseases. Unlike normal blood eosinophils, those that circulate in HES and those that infiltrate inflamed tissue exhibit an "activated" phenotype. To model intestinal epithelial-eosinophil interactions, we used peripheral blood eosinophils and human crypt-like T84 epithelial cell-line monolayers. Eosinophils from normal, mildly atopic donors, only if activated by PMA or primed with granulocyte-macrophage-CSF for 48 h, as well as eosinophils from HES patients elicited a short circuit current when applied apically to T84 monolayers. This eosinophil-derived bioactivity, which was transferable in cell-free supernatants and in < 1000 m.w. ultrafiltrates, stimulated electrogenic Cl- secretion, as indicated by inhibition with basolateral bumetanide or gluconate substitution and by enhancement of the rate constant for 125I efflux from preloaded T84 cells. This secretagogue activity was blocked in both intact activated eosinophils and in eosinophil-conditioned supernatants, by 8-phenyl-theophylline, indicating involvement of an adenosine receptor. Ion exchange and reversed-phase HPLC analyses demonstrated that eosinophil supernatant ultrafiltrates contained elevated levels of 5'-AMP that was converted to adenosine after incubation with epithelium. Inhibition of epithelial apical membrane ecto-5'-nucleotidase ablated the conversion to adenosine. These studies establish that activated eosinophils elicit Cl- secretion from intestinal epithelial and that 5'-AMP released by eosinophils followed by its conversion to adenosine at the epithelial surface is the basis for this response.

Adenosine Diphosphate↗
PubMed1993

Mast cells, neutrophils, and eosinophils in prurigo nodularis.

BACKGROUND AND DESIGN: Prurigo nodularis is a disease of unknown cause. To characterize the involvement of mast cells, neutrophils, and eosinophils in lesional tissue, we analyzed seven skin biopsy specimens by an indirect immunofluorescence technique for localization of mast cell tryptase, neutrophil elastase, and eosinophil granule major basic protein, eosinophil cationic protein, and eosinophil-derived neurotoxin. RESULTS: Mast cells were detected in all of the specimens, with prominent numbers of mast cells in three specimens; there was minimal or no extracellular deposition of tryptase in any of the tissues. Neutrophil infiltration was observed in all specimens, but few cells were observed in four; extracellular elastase was minimal or absent in all but one specimen in which prominent dermal elastase deposition was found. Scanty eosinophil infiltration was present in all specimens; however, extracellular deposition of the eosinophil granule proteins including major basic protein, eosinophil-derived neurotoxin, and eosinophil cationic protein was present in all but one specimen and striking deposition of at least one eosinophil granule protein was present in six of the seven specimens. CONCLUSIONS: These studies suggest that mast cell numbers are increased in prurigo nodularis and that eosinophil degranulation as evidenced by striking extracellular deposition of granule proteins is prominent in lesions. In contrast, extracellular deposition of mast cell and neutrophil proteins is absent. The distinctive proteins of the eosinophil granule have potent effects on tissues; the toxicity of these proteins and their deposition in lesional tissue suggest a pathogenic role for the eosinophil in prurigo nodularis.

Adult↗
PubMed1993

Increased protein kinase C activity in low density eosinophils.

Eosinophil heterogeneity is expressed in cell density, membrane receptors and function. It has been observed that increases in some functional activities correlate with decreased sedimentation density in human eosinophils. However, the cellular mechanisms to explain the up-regulation of eosinophil function have not been fully explored. Protein kinase C (PKC) is an important family of enzymes mediating signal transduction for a wide variety of functions in many different cell types. Changes in the activity of PKC could explain some of the observed differences in function. In these experiments, PKC activity of human granulocyte lysate supernatants was measured as the phosphatidyl serine-dependent transfer of 32P from [gamma-32P]ATP to a protein substrate under conditions of maximal stimulation; a measure of activatable PKC concentration. We observed that the activity present in eosinophils (87.2 +/- 8.4 pmol PO4 incorporated into histone per minute per 10(6) cells, n = 30) was not significantly different from that of neutrophils assayed under the same conditions (91.5 +/- 5.6 U, n = 31) but the percent of total activity that was phosphatidyl serine dependent was greater in eosinophils (97 +/- 1% vs 81 +/- 1% for neutrophils, p = 0.001). Blood eosinophils isolated from low density Percoll fractions had a higher activity (120 +/- 16 U) than that found in the higher density cells from the same subjects (81 +/- 19 U, n = 9, p = 0.011). When eosinophils recovered from bronchoalveolar lavage (BAL) fluid after segmental Ag challenges were assayed, the PKC activity of BAL eosinophils was similar to that of blood-derived eosinophils of equal density and low density BAL eosinophil PKC tended to be equal to or greater than higher density cells. The beta isozyme of PKC but not the alpha or gamma was detected in eosinophils by Western blotting with isozyme-specific mAb. These data indicate that eosinophil PKC activity is primarily caused by the beta-isozyme, is related to cell density in blood-derived cells, and may have a relationship to cell function.

Blotting, Western↗
PubMed1996

Activation of human eosinophils by IL-13. Induction of CD69 surface antigen, its relationship to messenger RNA expression, and promotion of cellular viability.

To study the effect of IL-13 on CD69 expression and cell viability in human eosinophils, purified human peripheral blood eosinophils from healthy donors were incubated with increasing concentrations of IL-13. The expression of CD69 was analyzed by flow cytometry (FACS). Surface expression of CD69, which was absent on untreated eosinophils, was induced by IL-13 at concentrations ranging from 1 ng/ml to 1 microgram/ml in a concentration-dependent manner. In contrast, neutrophils expressed CD69 neither spontaneously nor following incubation with IL-13. Semiquantitative reverse transcription-PCR for CD69 mRNA showed constitutive CD69 mRNA expression in purified human eosinophils. Incubation of eosinophils with IL-13 further increased CD69-specific mRNA. Analysis of intracellularly stored CD69 in eosinophils permeabilized with saponin revealed intracellular binding of anti-CD69 Abs in all isolated eosinophils. After stimulation with 100 ng/ml IL-13 for 24 h, the concentration of intracellular CD69 decreased by 41 +/- 9%. Furthermore, IL-13 at a concentration of 100 ng/ml enhanced eosinophil viability, as assessed by propidium iodide staining after 4 days in culture from 8.6 +/- 5.5% in control medium to 50.7 +/- 6.8% following stimulation with IL-13 treatment. The effect of Il-13 on eosinophil viability as well as that on CD69 expression were both neutralized by anti-IL-13 Abs. In conclusion, our results demonstrate that IL-13 specifically activates human eosinophils, as determined by the expression of CD69 cell surface protein and mRNA expression. Furthermore, IL-13 significantly prolongs eosinophil survival in vitro. The data suggest that IL-13 may play a role in the activation of eosinophils.

Antigens, CD↗
PubMed1996

Human eosinophils elaborate the lymphocyte chemoattractants. IL-16 (lymphocyte chemoattractant factor) and RANTES.

Eosinophils and CD4+ lymphocytes are preferentially recruited into sites of allergic inflammation. A role for eosinophils in the recruitment of CD4+ lymphocytes has not been defined. We studied the capacity of human eosinophils to release chemoattractants for T lymphocytes. Supernatants of cultured eosinophils contained chemoattractant activity for lymphocytes, which was predominantly due to IL-16 (lymphocyte chemoattractant factor) and RANTES. With neutralizing Abs, eosinophil-derived lymphocyte chemotactic activity was diminished by a mean (+/- SEM) of 60 +/- 3% with polygonal anti-IL-16 Ab, 69 +/- 4% with anti-IL-16 mAb, 48 +/- 3% with anti-CD4 F(ab) (IL-16 receptor blockade), 40 +/- 4% with anti-RANTES mAb, and 88 +/- 5% with a combination of anti-IL-16 and anti-RANTES mAbs. IL-16 and RANTES were detectable in eosinophil-derived supernatants by ELISA. Eosinophils constitutively expressed mRNA transcripts for both IL-16 and RANTES detectable by reverse transcription-PCR and contained preformed IL-16 and RANTES demonstrable by ELISA of cell lysates and by immunocytochemistry of freshly isolated eosinophils. Thus, eosinophils are a source of two cytokines, IL-16 and RANTES, that are chemoattractants for lymphocytes as well as eosinophils. These data indicate that eosinophils could contribute cytokines to enhance the recruitment of additional populations of CD4+ lymphocytes and eosinophils.

Antibodies, Monoclonal↗
PubMed1997

Characterization of eosinophil progenitor cells in feline bone marrow.

OBJECTIVE: To identify eosinophil progenitor cells in feline bone marrow, establishing an assay method to use in studies of eosinophilopoiesis and eosinophilopoietic factors in cats. ANIMALS: Healthy, laboratory animal source cats. PROCEDURE: Sources of colony-stimulating activity were prepared by conditioning media with bone marrow, spleen, and blood mononuclear cells from cats infected with Toxocara canis. Bone marrow cells were aspirated and cultured to develop the eosinophil progenitor cell assay and to test cells from 9 healthy cats in the assay. RESULTS: Optimal conditions for identifying colony-forming units-eosinophil and cluster-forming units-eosinophil were as follows. Bone marrow mononuclear cells (10(5)) were plated in 1 ml of supplemented medium, fetal bovine serum, and agar. The source of eosinophil growth factor(s) was bone marrow-conditioned medium made in the presence of 2.5 micrograms of concanavalin A/ml; other conditioned media also supported eosinophil colony growth. Dishes were incubated for 7 days at 37 C and 7% CO2. The colony-forming units-eosinophil formed aggregates of > 50 Luxol fast blue-positive cells and had dispersed morphology; the cluster-forming units-eosinophil formed aggregates of < 50 cells. CONCLUSION AND CLINICAL RELEVANCE: Similar to other species, cats have separate and distinct eosinophil progenitor cells. The eosinophil progenitor assay may be used to characterize altered kinetics of eosinophilopoiesis, to assess eosinophil growth factors, and to evaluate therapeutic regimens that might be useful in the management of excess eosinophil production.

Animals↗
PubMed2004

Allergen extracts directly mobilize and activate human eosinophils.

Allergic diseases are characterized by the presence of eosinophils, which are recruited to the affected tissues by chemoattractants produced by T cells, mast cells and epithelium. Our objective was to evaluate if allergens can directly activate human eosinophils. The capacity of purified allergen extracts to elicit eosinophil chemotaxis, respiratory burst, degranulation and up-regulation of the adhesion molecule complement receptor 3 (CR3) was determined in eosinophils isolated from healthy blood donors. Eosinophils stimulated with an extract from house dust mite (HDM) released the granule protein major basic protein (MBP) and up-regulated the surface expression of CR3. Cat allergen extracts also induced the up-regulation of CR3, but not the release of MBP; instead cat, as well as birch and grass allergens, elicited the release of eosinophil peroxidase (EPO). In addition, grass pollen extract caused the secretion of MBP. None of the allergens stimulated eosinophilic cationic protein release, nor production of free oxygen radicals. Both HDM and birch extracts were chemotactic for eosinophils. These findings establish that common aeroallergens can directly activate eosinophils in vitro. We propose that eosinophil activation in vivo is not exclusively mediated by cytokines and chemokines of the allergic inflammatory reaction, but could partly be the result of direct interaction between allergens and eosinophils.

Allergens↗
PubMed1999

Ursodeoxycholic acid inhibits eosinophil degranulation in patients with primary biliary cirrhosis.

Eosinophilia is a distinctive feature of primary biliary cirrhosis (PBC), especially in its early stages. Intriguingly, treatment with ursodeoxycholic acid (UDCA) ameliorates eosinophilia as well as liver tests in patients with PBC. It remains unknown, however, whether eosinophils in PBC patients are functionally activated and whether UDCA inhibits eosinophil activation. In the present study, we systematically examined eosinophil dynamics in the blood and liver in patients with stage I to II PBC before and after UDCA treatment. We determined serum concentrations of eosinophil granule proteins (major basic protein [MBP] and eosinophil-derived neurotoxin [EDN]) by radioimmunoassay and quantitated eosinophil degranulation using computer-assisted morphometry after MBP immunohistochemistry. Before UDCA treatment, patients with PBC (n = 25) showed significantly higher circulating eosinophil counts (P <. 05) and serum concentrations of MBP (P <.0005) and EDN (P <.02) compared with patients with chronic viral hepatitis (n = 22), autoimmune hepatitis (n = 10), and obstructive jaundice (n = 12). Four-week UDCA treatment significantly reduced blood eosinophil counts (P <.0001) and serum MBP (P <.0001) and EDN (P <.0001) levels in PBC patients. MBP immunohistochemistry and computer-assisted quantitative morphometry showed infiltration and degranulation of eosinophils in the portal tract in patients with PBC and significant reductions in the number of sites and the area occupied by extracellular MBP deposits after UDCA treatment for 2 years (P <.02) but not in placebo-treated patients. Our results suggest that eosinophils in patients with PBC are not only increased in number, but also release granule proteins, and that UDCA treatment inhibits this eosinophil activation/degranulation.

Blood Proteins↗
PubMed1998

Increased eosinophil activity in acute Plasmodium falciparum infection--association with cerebral malaria.

To assess the eosinophil response to Plasmodium falciparum infection a cohort of initially parasite-free Ghanaian children was followed for 3 months. Seven of nine children who acquired an asymptomatic P. falciparum infection showed increase in eosinophil counts, while a decrease was found in seven of nine children with symptomatic malaria, and no change was observed in 14 children who remained parasite-free. In a hospital-based study, paediatric patients with cerebral malaria (CM), severe anaemia (SA), or uncomplicated malaria (UM) had uniformly low eosinophil counts during the acute illness followed by eosinophilia 30 days after cure. Plasma levels of eosinophil cationic protein (ECP) and eosinophil protein X (EPX) were measured as indicators of eosinophil activation. In spite of the low eosinophil counts, ECP levels were increased on day 0 and significantly higher in patients with CM (geometric mean (95% confidence interval) 8.5 ng/ml (6.8-10.7 ng/ml)) than in SA (4.7 ng/ml (3.0-7.5 ng/ml)) and UM patients (4.3 ng/ml (3.6-5.3 ng/ml), P < 0.001). A similar pattern was found for EPX. It thus appears that the low eosinophil counts may be due to tissue sequestration and destruction rather than decreased production. The plasma levels of the granule proteins correlated with levels of tumour necrosis factor and soluble IL-2 receptor, implicating inflammatory responses and T cell activation as causes of the eosinophil activation. By contrast, the eosinophil induction did not appear to be part of a Th2-like response. Eosinophil granule proteins may be important in both control of malaria infection and the pathogenesis of severe malaria.

Animals↗
PubMed1994

Releasability of human hypereosinophilic eosinophils is related to the density of the cells.

The activity of eosinophils and neutrophils with respect to the release of granule proteins was studied in 11 patients with the hypereosinophilic syndrome (HES). Granulocytes or purified eosinophils were stimulated with serumopsonized Sephadex particles (C3b-induced release), and the released amounts of eosinophil cationic protein (ECP), eosinophils protein-X (EPX) and myeloperoxidase (MPO) were measured by means of specific radioimmunoassays (RIA). Eosinophils obtained from patients with HES released significantly more ECP (P < 0.002) and EPX (P < 0.01) after 20 min of incubation than cells from the control group. The cellular content of ECP and EPX in eosinophils obtained from the patients with HES was significantly reduced to 50% and 62%, respectively, of the content of these granule proteins of eosinophils from the control group. In separated eosinophils light-density eosinophils released more of both ECP and EPX than normal density eosinophils. There was no difference in MPO release between the patients and the control group. We conclude that the eosinophils from patients with HES have an increased propensity to release their granule proteins and the releasability seems to be related to the density of the cells.

Adolescent↗
PubMed1996

Isolation and characterization of porcine cationic eosinophil granule proteins.

The allergic pig can be used as a large-animal model for studies of allergic reactions in the airways and the role of eosinophils in such reactions. To measure the activation of eosinophils, the release of eosinophil-derived cationic proteins can be used. The purpose of this study was to isolate and characterize cationic proteins derived from porcine eosinophils. Pigs were infested with live Ascaris suum eggs to induce eosinophilia (greater than or = 40% of leukocytes). Blood was collected and leukocytes were prepared by dextran sedimentation. Granules were obtained from the homogenized leukocytes by ultracentrifugation and cationic proteins were extracted and separated by gel filtration, cation exchange and zinc affinity chromatography. Using these methods, three cationic proteins were isolated from pig granulocytes, two of which were shown to originate from the eosinophil. The proteins were characterized according to molecular weight, amino acid composition, N-terminal sequence, isoelectric point, peroxidase and ribonuclease activity and antigenicity. One eosinophil protein was identified as eosinophil peroxidase and the other showed great similarities with human eosinophil cationic protein. The third protein was not specific for eosinophils, and had no obvious equivalent in human granulocytes. The eosinophil-derived proteins may be useful in the studies of eosinophil activation, e.g. in late-phase asthmatic reactions, where the pig represents a new candidate model for large-animal allergy research.

Amino Acid Sequence↗
PubMed1991

Functional heterogeneity of human eosinophil chemotactic lymphokines.

We have previously isolated two OKT4-positive T lymphocyte-derived eosinophil chemotactic factors (LDECF) with MW of about 45-60 kDa of which production is different in antigen or mitogen dependency (1-4). The production of a LDECF from patients with parasite disease (LDECF-PD) is dependent on antigen or mitogen stimulation, whereas another LDECF from patients with hypereosinophilic syndrome (HES) is independent. Further purification of these LDECF with isoelectric focusing reveals that an isoelectric point of LDECF-HES is about 6.0 and that of LDECF-PD is around 7.0 to 8.0. Little or no activity of partially purified LDECF-HES and LDECF-PD is suppressed by treatment with monoclonal antibodies against GM-CSM, IL-3, and IL-5, which activate eosinophils. LDECF-HES and LDECF-PD attract eosinophils from healthy individuals. In contrast, eosinophils from patients with HES are attracted by LDECF-HES but not LDECF-PD. LDECF-HES enhances the expression of Fc epsilon receptor II (Fc epsilon RII) and Fc gamma receptor III (Fc gamma RIII) but not that of CR1 on eosinophils, whereas LDECF-PD enhances their CR1 and Fc gamma RIII expression but not Fc epsilon RII expression. Moreover, treatment with LDECF-PD suppresses the release of eosinophilic cationic protein (ECP) from eosinophils, whereas that with LDECF-HES fails. Treatment of eosinophils with phorbol myristate acetate enhances ECP release from eosinophils but it fails to enhance the intracellular ECP level. However, the intracellular ECP level is elevated by stimulation with phorbol myristate acetate if eosinophils were previously treated with LDECF-HES but not with LDECF-PD. These results suggest that various kinds of LDECF are produced according to the nature of diseases, and that each LDECF has functional heterogeneity on eosinophils.

Antigens, Surface↗
PubMed2003

Expression of RANTES mRNA in skin lesions of feline eosinophilic plaque.

One of the mechanisms of eosinophil infiltration is its induction by chemoattractants such as regulated upon activation, normal T-expressed and secreted (RANTES) which is a cysteine-cysteine chemokine that mediates chemotaxis and activation of eosinophils in humans and mice. Skin lesions of feline eosinophilic plaque are characterized by a predominant infiltration of eosinophils. The mechanism(s) of eosinophilic infiltration in the skin and/or mucosa of cats is unknown. It is possible that RANTES is involved. To investigate the presence of RANTES in the skin of cats with eosinophilic plaques and nonaffected skin, we cloned and sequenced the full-length feline RANTES cDNA gene, in order to determine whether it is present in the skin of cats with eosinophilic plaques and/or if it is present in normal adjacent skin. We were able to document the the expression of RANTES mRNAs in skin with feline eosinophilic plaque as well as in normal cat skin. The full-length cDNA sequence of the RANTES gene (742 bp) contained a single open reading frame of 276 bp encoding a protein of 92 amino acids. The amino acid sequence of feline RANTES shared 67 and 74% sequence identity with that of bovine and mouse RANTES genes, respectively. RT-PCR analysis on RANTES mRNA in the skin of cats with eosinophilic plaque revealed that its expression was higher in the eosinophilic plaque skin lesions than in the normal skin. The result suggested that RANTES might play a role to induce eosinophil infiltration in feline eosinophilic plaque lesions.

Amino Acid Sequence↗