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At least 343 records · Page 19Linked to original sources
PubMed1991

Analysis of the survival of mature human eosinophils: interleukin-5 prevents apoptosis in mature human eosinophils.

We and other groups have previously shown that interleukin-5 (IL-5) maintained the viability of mature eosinophils in an in vitro liquid culture system. Mature eosinophils did not proliferate but their survival was maintained in the presence of IL-5. Using this culture system, we investigated the mechanism of IL-5-mediated survival. In the absence of human IL-5 (hIL-5) mature eosinophils succumbed after 4 days, while in the presence of hIL-5 they survived up to 10 days. When DNA extracts of cultured eosinophils were analyzed on an agar gel electrophoresis, marked DNA fragmentation was observed in the absence of hIL-5, while no significant DNA fragmentation was observed in the culture with hIL-5 for 48 hours. The DNA fragmentation appeared as early as 6 to 12 hours after hIL-5 deprivation. Concomitantly, IL-5 stimulated total RNA and protein synthesis, but did not induce DNA synthesis in mature eosinophils. Because cycloheximide or actinomycin D impeded the protection of apoptosis by hIL-5, some new RNA and protein synthesis appeared to be required in this phenomena. These findings indicate that IL-5 maintains survival of mature eosinophils with induction of new RNA and protein synthesis, thus leading to the inhibition of apoptosis.

Cell Death↗
PubMed1991

[Hypodense eosinophils are much labeled with 32P than normodense eosinophils].

Peripheral blood eosinophils from the patients with atopic dermatitis were isolated on a Percoll gradient and incubated with H3(32)PO4. After stopping the reaction, SDS/PAG electrophoresis was performed and autoradiographs were prepared to determine the incorporation of 32P into proteins. Eosinophils developed at least 14 protein bands below 66.2 K by SDS/PAG electrophoresis and the differences of the staining patterns between hypodense and normodense eosinophils were observed. In the autoradiographs 5 distinct radioactive bands were observed below 31 K. 32P incorporation into the bands of hypodense eosinophils were stronger than that of normodense eosinophils, suggesting possible involvement of protein phosphorylation in the activation process of eosinophils.

Adult↗
PubMed1982

Bullous pemphigoid blister fluid stimulates eosinophil colony formation and activates eosinophils.

An eosinophil stimulating material (ESM) is described in the blister fluids (BF) of six patients with bullous pemphigoid (BP). This ESM is similar in function to a subspecies of human colony stimulating factor (CSF), CSF-alpha, since (i) it stimulated the production from bone marrow cells of day 14 colonies (31 +/- 15, arithmetic mean +/- 1 s.e.m. colonies, n = 5) in semi-solid agar, (ii) a large proportion (47 +/- 12%, n = 5) of these colonies were eosinophilic and (iii) it activated purified peripheral eosinophils as judged by increased autofluorescence (a mean increase of 23.6 +/- 6.6 units measured by flow cytometry, n = 10). BF from patients with four other blistering diseases, burn blisters, suction blisters from normal, eosinophilic or BP patients, various sera, histamine and eosinophil chemotactic factor (ECF-A) lacked activities in these assays. This description of a tissue accumulation of a CSF like substance suggests that there exists a physiological role for CSF in the periphery. In addition it supports the concept that local activation of eosinophils contributes to the pathogenesis of BP.

Aged↗
PubMed1982

Complement-mediated leukocyte adherence to infective larvae of Dipetalonema viteae (Filarioidea): requirement for eosinophils or eosinophil products in effecting macrophage adherence.

The present study reports the existence of C-mediated adherence of eosinophils and/or macrophages to filarial infective larvae of Dipetalonema viteae. C3 molecules are present on the surface of the parasite, as shown by immunofluorescence studies. Samples of fNRS depleted of AP of complement by treatment with Zymosan A or of factor B by heating at 50 degrees C for 20 min fail to mediate cell adherence to the parasite. In contrast, fNRS inactivated for CP of complement by the chelating agent EGTA retains its activity in mediating cell adherence to the parasite. There is a significant consumption of factor B and AP of complement when infective larvae are incubated in fNHS. Consumption of C4 of the CP of complement is much lower in the same test. The adherence of macrophages cannot occur without the simultaneous presence of eosinophils, whereas eosinophils probably act alone and not in concert with macrophages. The eosinophil adherence is associated with degranulation. The damage is notably enhanced by replacing the spent eosinophil population with a newly obtained population. In the present test system, mast cells did not adhere to filarial larvae even when mast cell-rich populations were used, nor did they effect macrophage adherence when presented in association with the latter. When eosinophil-enriched cell populations containing less than 1% mast cells were used, cell adherence to filarial larvae still occurred, but the presence of 30% mast cells in such cell populations markedly increased both the rate and level of adherence. We suggest that a cell-mediated adherence and destruction dependent upon the activation of complement via AP, without a requirement for specific antibody, may represent a natural mechanism of parasite killing in a nonimmune host.

Animals↗
PubMed1995

[Effect of rantes (regulated on activation, normal T expressed and secreted) on eosinophil adhesion to plasma coated glass using eosinophilic cell line (EoL-1)].

Recently, adhesion molecules expressed on various inflammatory cells, especially on eosinophils are considered to play an important role in allergic inflammation such as bronchial asthma. RANTES (Regulated on activation normal T expressed and secreted) seems to be the most important chemokine which belongs to Platelet factor 4 (PF4) superfamily, since RANTES is revealed as a chemotactic factor for eosinophils as well as memory T cells or monocytes. In this study, we examined the effect of RANTES on eosinophil adhesion to plasma coated glass using eosinophilic cell line named EoL-1. RANTES augmented EoL-1 adherence to Plasma coated glass and EoL-1 adherence to plasma coated glass was inhibited by anti-VLA-4 antibody, anti-CR3 antibody. On the other hand, RANTES did not augment expression of adhesion molecules (VLA-4, CR3) on EoL-1. These findings indicate that RANTES intensify the adhesion of eosinophils without augmentation of their expression, and suggest that it induce qualitative, but not quantitative changes in their adherence. Taken together, our study suggest that RANTES up-regulates the inflammatory reaction through augmentative effect on adhesion of eosinophils in bronchial asthma.

Cell Adhesion↗
PubMed1994

[Effect of platelet-activating factor (PAF) on eosinophil adhesion to plasma-coated glass using eosinophilic cell lines (EoL-1, EoL-3)].

Adhesion molecules on various inflammatory cells, especially on eosinophils are now considered to play an important role in allergic inflammations such as bronchial asthma. In this study, we examined the effect of platelet-activating factor (PAF) on eosinophil adhesion to plasma-coated glass using eosinophilic cell lines (EoL-1, EoL-3), since PAF might be an important mediator as an eosinophil chemotactic agent in bronchial asthma. PAF markedly augmented adherence to plasma-coated plates. This finding suggests that PAF might up-regulate the inflammatory reaction in bronchial asthma through its action as an augmentative agent for eosinophil adhesion as well as its action as an eosinophil chemotactic agent.

Cell Adhesion↗
PubMed1993

[Ring eosinophils in patients with lowered eosinophil peroxidase activity].

Leucocyte cytograms were obtained by using a Technicon H6000 (Technicon Instrument Corporation, Tarrytown, NY, USA) in conjunction with an automated flow-cytochemical analyser by which leucocytes can be differentiated by cytochemical (peroxidase activity) and optical (cell size) methods. By analysis of cytograms obtained in this way, we found twelve cases of lowered eosinophil peroxidase activity among approximately 600,000 blood samples-days between 1984 and 1989. Ring eosinophils were observed on the peripheral blood smears in 2 out of 12 cases. The first case was a 41-year-old female confined to hospital with Hashimoto's disease, and the other a 54-year-old female hospitalized for trauma. In both cases, the percentage of eosinophils was normal, although some had ring-shaped nuclei with a large central nuclear hole and a nuclear ring formed with a thin nuclear chromatin bridge. Ring eosinophils previously have been described in patients with hematological malignancy, hypereosinophilic syndrome or severe alcoholism. Recently we observed ring eosinophils in a healthy individual for the first time. Although ring eosinophils may not have specific diagnostic significance, these cases are reported because they displayed a rare phenomenon.

Adolescent↗
PubMed1993

Platelet-activating factor-induced human eosinophil activation. Generation and release of cyclo-oxygenase metabolites in human blood eosinophils from asthmatics.

The spontaneous and stimulated generation of fatty acid cyclo-oxygenase pathway-derived products of arachidonic acid from highly purified (91.6 +/- 1.3%, n = 23) human blood eosinophils obtained from asthmatics were examined using combined gas chromatography/mass spectrometry. Under resting conditions, eosinophils spontaneously generated 0.24 +/- 0.10 pg prostaglandin E2 (PGE2), 0.51 +/- 0.20 prostaglandin D2 (PGD2), 0.35 +/- 0.10 pg prostaglandin F2 alpha (PGF2 alpha) and 8.5 +/- 2.2 pg thromboxane B2 (TXB2), the stable metabolite of TXA2 per 10(6) cells. In contrast, 6-keto-prostaglandin F1 alpha and 9 alpha,11 beta-prostaglandin F2 were not detectable. Stimulation of eosinophils with platelet-activating factor (PAF) for 5 min induced a two- to sixfold increase in the biosynthesis of prostanoids. More than 95% of the generated prostanoids were released into the surrounding medium. The response to PAF was inhibited by the PAF receptor antagonist WEB 2086 (1 microM). The fatty acid cyclo-oxygenase inhibitor, ibuprofen, abolished both the spontaneous and PAF-stimulated generation of prostanoids by eosinophils. LTB4, PMA and calcimycin also produced an increase in prostanoid production, whereas lyso-PAF, the PAF precursor and metabolite, failed to induce prostanoid generation over basal production. In conclusion, the results demonstrate that PAF potently activates human eosinophils to generate and release several fatty acid cyclo-oxygenase metabolites of the arachidonic acid pathway, with TXB2 being the most abundant. These data are in agreement with previous observations suggesting that PAF may be an important stimulus for prostanoid release by the eosinophil in allergic diseases such as asthma.

Asthma↗
PubMed1993

Inhibitory effects of azelastine hydrochloride on Ca2+ influx, actin polymerization and release of eosinophil cationic protein of an eosinophilic leukaemia cell line EoL-1.

The inhibitory effects of azelastine hydrochloride on PAF-induced and fMLP-induced Ca2+ influx, actin polymerization and calcium ionophore A23187-induced and aggregated IgG-induced release of eosinophil cationic protein (ECP) of an eosinophilic leukaemia cell line, EoL-1, were examined. EoL-1 cells cultured with 0.2 mM dibutyryladenosine-cyclic monophosphate for 48 hours showed an increase in intracellular free Ca2+ concentration ([Ca2+]i) and actin polymerization when stimulated by PAF and fMLP. Azelastine hydrochloride inhibited PAF-induced and fMLP-induced Ca2+ influx ([Ca2+]i) in a dose-dependent manner with an IC50 of 1 x 10(-8) M and 1 x 10(-7) M, respectively. It also inhibited PAF-induced and fMLP-induced actin polymerization in a dose-dependent manner up to 40% and 30%, respectively. EoL-1 cells were differentiated to contain ECP in their eosinophilic granules when cultured for 9 days with supernatants of a human adult T cell leukaemia cell line, HIL-3 (HIL-3 sup). Calcium ionophore A23187 and aggregated IgG induced the secretion of ECP by EoL-1 cells. Azelastine hydrochloride inhibited the secretion of ECP in a dose-dependent manner. These inhibitory effects were seen even at therapeutic concentrations of 10(-8) M to 10(-9) M. These results indicate that the therapeutic effects of azelastine hydrochloride as an anti-allergic agent may include inhibition of the accumulation of eosinophils into the locus of allergic inflammation and of the release of cytotoxic granules from eosinophils.

Actins↗
PubMed1990

Eosinophilic ureteritis associated with eosinophilic cholangitis: a case report.

Eosinophilic infiltrate of the urinary tract is rare. We report on a patient with eosinophilic cholangitis who later had eosinophilic ureteritis. This case emphasizes the potential serious nature of eosinophilic ureteritis, which often presents with complete ureteral obstruction. The literature pertaining to eosinophilic ureteritis and eosinophilic biliary disease is reviewed.

Bile Ducts↗
PubMed1977

[Paraneoplastic eosinophilic leukemoid with eosinophilic parietal thromboendocarditis in malignant melanoma].

A case of an eosinophilic leukemoid reaction associated with metastasizing malignant melanoma and thrombotic eosinophilic parietal endocarditis in a 58-year-old white male is reported. No similar cases were found in the literature. The leukemoid reaction with leukocytosis of up to 102 300 white cells per microliter , 65% of which were eosinophils, was observed during the last two months of life of the patient, who died of multiple metastasis of malignant melanoma. The primary malignant melanoma had been excised four years before death. The parietal endocarditis was localized on the posterior wall of the left ventricle and was found incidentally at autopsy. The association of leukemoid eosinophilic reaction with consecutive eosinophilic thrombotic parietal endocarditis is believed to be part of a paraneoplastic syndrome. 63 published cases of paraneoplastic eosinophilic leukemoid reaction and 6 published cases of malignant tumor with eosinophilia and additional parietal endocarditis were found. The pathogenesis of these conditions is discussed.

Endocarditis↗
PubMed1989

Preparation and characterization of monoclonal antibodies to human neutrophil cathepsin G, lactoferrin, eosinophil peroxidase, and eosinophil major basic protein.

This report describes the production and characterization of five murine monoclonal antibodies that react with granule proteins of human granulocytes. Monoclonal antibody AHN-11 (IgG2a) reacted specifically with neutrophil cathepsin G; no reactivity with the homologous neutrophil neutral proteases, elastase, proteinase 3, or esterase N was detected. Antibodies AHN-9 (IgG1) and AHN-9.1 (IgG2b) each reacted with different epitopes on human lactoferrin, but not with the homologous protein transferrin. Two IgG1 antibodies, AHE-1 and AHE-2, reacted specifically with eosinophils; AHE-1 reacted strongly with eosinophil peroxidase but not eosinophil major basic protein while AHE-2 recognized eosinophil major basic protein but not eosinophil peroxidase. All five antibodies could detect their respective antigens in alcohol-fixed cytospin preparations. These antibodies should be useful for immunolocalization and quantification of their respective antigens as well as for other studies of the roles of these proteins in granulocyte function and differentiation.

Antibodies, Monoclonal↗
PubMed2002

Infiltrating eosinophils and eotaxin: their association with idiopathic eosinophilic esophagitis.

BACKGROUND: Idiopathic eosinophilic esophagitis (IEE) is a very rare disease characterized by thickening and eosinophil infiltration of the esophagus. The most potent chemotactic factor for eosinophils is eotaxin, and its pathophysiologic significance in IEE needs to be elucidated. OBJECTIVE: To study the association between eotaxin and IEE. METHODS: We examined eotaxin expression in the esophagus of an IEE patient in comparison to controls by immunohistochemistry using a monoclonal antibody for human eotaxin. We also measured the free eotaxin level and the total (free and bound-form) eotaxin level in blood by enzyme-linked immunosorbent assay before and after the initiation of steroid therapy. RESULTS: Most of the infiltrating eosinophils in the affected esophageal tissue showed immunohistochemical staining with anti-eotaxin antibody. In blood samples, the free eotaxin level was slightly elevated before treatment, whereas the total eotaxin level was within the normal range. Unexpectedly, the total eotaxin level increased dramatically after the initiation of steroid therapy, whereas the increase of free eotaxin was modest. CONCLUSION: Infiltrating eosinophils that express eotaxin and the changes of blood eotaxin levels during steroid therapy suggest that eotaxin may be associated with IEE.

Chemokine CCL11↗
PubMed2000

Eosinophil cationic protein and eosinophil protein X in the nasal lavage of children during the first 4 weeks of life. SPACE Collaborative Study Team.

Eosinophil cationic protein (ECP) and eosinophil protein X (EPX) are well established as markers of eosinophil activation. We analyzed ECP and EPX concentrations in nasal lavage fluids (NALF) of 378 neonates during their first 4 weeks of life. Inclusion criteria were a positive history of parental allergy and a positive skin prick test or specific IgE (RAST class > or = 2) against at least one out of a panel of common aeroallergens in one or both parents. Twenty-four infants with no history of parental allergy were used as controls. A volume of 2 ml of 0.9% saline was instilled into each nostril and immediately recovered by a suction device. ECP and EPX were analyzed by radioimmunoassay. In 65 samples of three consecutive lavages, EPX was detected in nine samples (13.8%) in the control group, whereas it was detected in 197/360 samples (54.7%) in the study population. The corresponding figures for ECP were 17/65 (26.2%) in the control group and 173/365 (47.4%) in the study group. Both proteins showed a skewed distribution (median/5-95th percentiles for ECP: 0 microg/l [0-69.4] and EPX: 6.6 microg/l [0-73.2]). The differences between the control group and the study group were statistically significant, regardless of the allergic disease of the parents. In children of allergic parents, activation proteins of the eosinophil granulocyte are released on the nasal mucosal surface in about 50% of the studied population at the age of 4 weeks. This early onset of eosinophil activation in the nasal respiratory epithelium may reflect a genetic predisposition to allergy or early exposure to allergens.

Blood Proteins↗
PubMed2004

Sputum eosinophil counts and eosinophil cationic protein levels in cough-variant asthma and in classic asthma, and their relationships to airway hypersensitivity or maximal airway response to methacholine.

BACKGROUND: The aims of this study were to compare the degree of airway inflammation in cough-variant asthma (CVA) with that in classic asthma (CA), and to examine the relationship between airway inflammation and airway hypersensitivity or maximal airway response to methacholine in both conditions. METHODS: Sputum was induced in 41 CVA patients, in 41 methacholine PC(20)-matched CA patients, and in 20 healthy children. The sputum samples were analyzed for total and differential cell counts, and for eosinophilic cationic protein (ECP). A high-dose methacholine challenge test was performed in CVA and CA patients to determine PC(20) and maximal airway response. RESULTS: Sputum eosinophil percentages and ECP levels were significantly elevated in CVA and CA vs the control, but no significant differences were found between the two asthma groups. In the two asthma groups, neither sputum parameters correlated significantly with methacholine PC(20). However, the absence of a maximal response plateau or its higher level, when present, was associated with increased eosinophil percentages and ECP levels in the CVA group. CONCLUSIONS: The degree of eosinophilic inflammation may not be causally related to differences in presented asthma manifestations. The identification of a maximal response plateau and the level of this plateau in patients with CVA may provide information pertinent to airway eosinophilic inflammation.

Adolescent↗
PubMed1995

Isolation and partial characterization of eosinophil granule proteins in rats--eosinophil cationic protein and major basic protein.

Peritoneal eosinophilia was induced in rats using Ascaris suum extract as an antigen, and characteristics of granule proteins of eosinophils collected from the peritoneal cavity were investigated. Peritoneal eosinophilia was induced by injection of the antigen solution into the peritoneal cavity of the immunized rats that had been orally administered with cyclophosphamide. Peritoneal cells were collected 48 h after injection of the antigen solution, incubated in plastic dishes, and nonadherent cells were collected as an eosinophil-rich fraction, from which granule proteins were extracted. Granule proteins were then purified by cation exchange chromatography, gel filtration, copper chelate affinity chromatography, and reverse-phase HPLC. Two distinct basic proteins of which molecular weights are 18- and 17-kD were obtained. Partial N-terminal amino acid sequence analysis revealed that the 18-kD protein and the 17-kD protein were homologous to the human eosinophil cationic protein (ECP) and the human and guinea pig major basic protein (MBP), respectively. Both the two proteins showed strong bactericidal activity against Escherichia coli and Staphylococcus aureus. These results indicate that rat eosinophils also possess ECP and MBP in their granules as well as human and guinea pig eosinophils.

Amino Acid Sequence↗
PubMed1992

Correlation of eosinophils, eosinophil cationic protein and soluble interleukin-2 receptor with the clinical activity of atopic dermatitis.

To evaluate the correlation with the clinical activity of atopic dermatitis (AD) we investigated prospectively cellular and serological parameters such as eosinophils, eosinophil cationic protein (ECP), soluble IL-2 receptor (sIL-2R), soluble CD23 (sCD23) and lactate dehydrogenase (LDH) in peripheral blood of 37 AD patients on admission to and discharge from the Department of Dermatology at the University Hospital in Zurich. On admission the actual clinical skin condition as measured by the skin intensity score (SIS) was significantly correlated with eosinophils (p less than 0.005), ECP (p less than 0.05) and sIL-2R (p less than 0.001). During the observation period a significant improvement in the clinical status as measured by the SIS was observed in all AD patients (p less than 0.001). A significant decrease in sIL-2R (p less than 0.005), which was most pronounced in the group of AD patients receiving systemic steroids, together with a decrease in eosinophils and ECP but not in sCD23 and LDH could be demonstrated between admission and discharge. In addition, a slight but significant increase in peripheral blood lymphocytes (p less than 0.005) and monocytes (p less than 0.01) was noted. Comparing the 'extrinsic' (n = 32) and the 'intrinsic' (n = 5) types of AD no significant differences with regard to the above mentioned parameters were found. Our data indicate that cellular and serological parameters such as eosinophils, ECP and sIL-2R reflect the clinical activity of AD and may therefore give further insights into the pathogenesis of this disease.

Adolescent↗
PubMed2000

Regulatory mechanism of eosinophil peroxidase release from guinea pig eosinophils.

The regulatory mechanism of degranulation of guinea pig peritoneal eosinophils was studied by determination of eosinophil peroxidase (EPO) release. Beta-agonists, such as isoproterenol, salbutamol and fenoterol, effectively inhibited A23187-induced EPO release from guinea pig eosinophils. The inhibitory effects of beta-agonists were attenuated by pretreatment with either propranolol, a non-selective beta-antagonist, or ICI 118,551, a selective beta2-antagonist. Both theophylline and dibutyryl-cAMP (db-cAMP) also significantly inhibited A23187-induced EPO release. The inhibition of EPO release induced by db-cAMP was attenuated by pretreatment with KT5720, a protein kinase A inhibitor. In addition, calphostin C as well as cytochalasin D effectively inhibited A23187-induced EPO release. From the results of the present study, it was concluded that an increase in intracellular Ca2+ concentration may lead to exocytosis of eosinophil granules through activation of protein kinase C and microfilaments. Beta-agonists and theophylline were effective in inhibiting degranulation of eosinophils by increasing intracellular cAMP level coupled with the activation of protein kinase A.

Adrenergic beta-Agonists↗