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PubMed1996

Patients with psoriasis have elevated levels of serum eosinophil cationic protein and increased numbers of EG2 positive eosinophils in the duodenal stroma.

The occurrence of EG2-positive (EG2+) eosinophils and IgE in biopsy specimens of duodenal mucosa and skin from 39 psoriasis patients was studied, with emphasis on the relation to serum eosinophil cationic protein (ECP), serum IgE and the presence or absence of serum IgA and IgG antigliadin antibodies. Psoriasis patients had significantly elevated serum levels of ECP even after exclusion of five of 37 sera which were Phadiatop positive. The elevated serum ECP was not associated with the presence of IgA or IgG antibodies to gliadin. After exclusion of Phadiatop positive sera the serum IgE values did not differ from those of a group of healthy blood donors. Patients with psoriasis had a pronounced increase of EG2+ cells in their duodenal stroma. Patients without antibodies to gliadin tended to have even more EG2+ cells than those with such antibodies and those with increased duodenal intraepithelial lymphocytes. IgE+ cells were present in most duodenal specimens, and in some specimens there were > 100 IgE+ cells/section. The number of EG2+ cells was increased in lesional skin and, in some patients, also in non-involved skin, but there was a more pronounced increase in EG2 reactivity in the duodenal than in the skin specimens. IgE reactivity was increased both in non-involved and involved skin and was significantly related to the number of IgE-positive cells in the duodenal stroma. The results of this study indicate that the gastrointestinal tract and the eosinophil granulocyte might be involved in psoriasis in a hitherto unknown way.

Adult↗

PubMed1998

Mechanisms of transcription in eosinophils: GATA-1, but not GATA-2, transactivates the promoter of the eosinophil granule major basic protein gene.

Granule major basic protein (MBP) is expressed exclusively in eosinophils, basophils, and placental trophoblasts. To identify the cis-elements and transcription factors involved in regulating MBP expression, we subcloned 3.2 kb of sequence upstream of the exon 9 transcriptional start site (P2 promoter) and serial 5' deletions into the pXP2 luciferase reporter vector. An 80% decrement in promoter activity was obtained when MBP sequences between bp -117 to -67 were deleted. To identify transcription factors that bind to and transactivate through the bp -117 to -67 region, we first compared the upstream genomic sequences of human and murine MBP; a potential GATA binding consensus site was conserved in the 50-bp region between the two genes. To determine which GATA proteins bind this consensus site, we performed electrophoretic mobility shift assays (EMSAs), which showed that both GATA-1 and GATA-2 can bind to this consensus site. To determine the functionality of this site, we tested whether GATA-1 and GATA-2, either individually or in combination, can transactivate the MBP promoter in the Jurkat T cell line. Cotransfection with a GATA-1 expression vector produced 20-fold augmentation of MBP promoter activity, whereas GATA-2 had no activity. In contrast, combined cotransfection of GATA-1 and GATA-2 decreased the ability of GATA-1 to transactivate the MBP promoter by approximately 50%. Our results provide the first evidence for a GATA-1 target gene in eosinophils, a negative regulatory role for GATA-2 in MBP expression, and possibly eosinophil gene transcription in general during myelopoiesis.

Binding Sites↗

PubMed1976

[3 cases of eosinophilic leukemia with atypical granulation in the eosinophils and neutrophils].

Three patients with eosinophilic leukemia and atypical granulation in the eosinophils are described. A remarkable light and electron microscopic finding was the appearance of enormous granules in the neurtophils and eosinophils. In addition the usual anomalies seen in acute leukemia, for example asynchronisation in cell maturation, fibrillar bundles, shrinkage of nucleolus and cell organelles, signs of degeneration and also the auer-rods characteristic of AML are observed.

Acute Disease↗

PubMed2003

Mast cell and eosinophils in the wall of the gut and eosinophils in the blood stream during Toxocara vitulorum infection of the water buffalo calves (Bubalus bubalis).

Toxocara vitulorum is a pathogenic nematode from the small intestine of very young buffalo calves. To understand the development of the inflammatory responses in the wall of the gut, samples of tissues were removed from the duodenum, jejunum and ileum of buffalo calves naturally infected with T. vitulorum during the beginning of the infection, at the peak of egg output, as well as during the periods of rejection of the worms and post-rejection. Two additional control groups of uninfected calves (by anti-helminthic therapy of their mothers and after the birth) were also necropsied on days 30 and 50 after birth. Blood samples were fortnightly collected from birth to 174 days post-birth. Blood smears were prepared and stained with Giemsa for eosinophils. The parasitological status of buffalo calves was evaluated through weekly fecal egg counts (EPG) from 1 to 106 days after birth, which revealed that T. vitulorum egg shedding started on day 11, reached the peak of the infection on day 49 and finally expelled the parasites between days 50 and 85 after birth. In the infected buffalo calves, the mast cell population increased significantly, by two-fold in the mucosa (villus-crypt unit (VCU)) of the duodenum and four-fold in the proximal jejunum; but these increases were statistically significant only at the peak of the infection. Although mast cell numbers increased in the mucosa of the ileum as well as in both the submucosal and muscle tissues of the duodenum, proximal jejunum and ileum, the data was not significantly different from the controls. Eosinophil numbers increased in the mucosa of the duodenum (two-five times higher than the control) and proximal jejunum (three-five-fold) during the period of the infection (beginning, peak and rejection). The relative numbers of eosinophils increased in the blood stream from the second to the seventh week. In conclusion, T. vitulorum infection elicited mastocytosis and tissue eosinophilia in the duodenum and proximal jejunum, as well as eosinophilia in the blood stream, during the beginning, at the peak and during the rejection of the worm. After the rejection of the worms, the numbers of these cells returned to normal levels suggesting that these cells may have a role in the process of rejection of T. vitulorum by the host.

Animals↗

PubMed1997

Intronic enhancer activity of the eosinophil-derived neurotoxin (RNS2) and eosinophil cationic protein (RNS3) genes is mediated by an NFAT-1 consensus binding sequence.

The eosinophil-derived neurotoxin (EDN) and eosinophil cationic protein (ECP) are both small, cationic ribonuclease toxins that are stored in and secreted by activated human eosinophilic leukocytes. We have previously shown that optimal expression of the EDN gene is dependent on an interaction between an intronic enhancer element or elements and the 5' promoter region. Here we present evidence demonstrating that the gene encoding ECP is regulated in an analogous fashion and that an intronic enhancer element functioning in both genes is a consensus binding sequence for the transcription factor NFAT-1. Our initial results demonstrate that one or more nuclear proteins isolated from human promyelocytic leukemia (HL-60) cells bind specifically at this consensus site (5'-GGAGAA-3') within the intron of the EDN gene and that disruption of this sequence reduced the characteristic 20-30-fold increase in reporter gene activity observed with the tandem EDN promoter/exon 1/intron construct to background levels. The NFAT-1 consensus site in the ECP gene differs from that found in the EDN gene by a single nucleotide (5'-GGAGAG-3'); the conversion of the 3' G to an A resulted in a further enhancement of the reporter gene activity supported by the ECP promoter/exon 1/intron construct. Interestingly, no "supershift" was observed in gel shift assays performed in the presence of anti-NFAT-1 antiserum, suggesting that a nuclear protein other than NFAT-1 may be acting at this consensus site.

Base Sequence↗

PubMed2006

Correlation between rheumatoid factor and peripheral eosinophil count in chronic eosinophilic pneumonia.

The relationship between the blood level of rheumatoid factor (RF) and the peripheral blood eosinophil (Eo) count (white blood cellsx%Eo, Eo count) in a patient diagnosed with chronic eosinophilic pneumonia was evaluated from before the onset till resolution of the disease. RF levels correlated with Eo counts, and showed a strong correlation with the logarithmic value of the Eo counts (r=0.816). RF levels tended to become elevated earlier and decline later than Eo counts or abnormal X-ray shadows. We concluded that the RF level may reflect the activity of this disease. The mechanism of RF elevation in eosinophil-activated disorders needs to be clarified.

Aged↗

PubMedDate not supplied

[Eosinophilic granulocytes: from common residents in normal gastrointestinal mucosa to aggressive agents of eosinophilic gastroenteritis].

Because of their biological affinity for normal gastrointestinal (GI) mucosa, eosinophilic granulocytes are "normal residents" in the mucosa. This physiological GI eosinophilia translates into a state of "permanent normal inflammation", which means that the mucosa's local immune system is constantly confronted by dietary proteins and indigenous microorganisms. This eosinophilic infiltration of the GI mucosa is increased, reactively, in the course of local inflammatory processes, collagenosis, infections (especially helminthic infections), vasculitis, neoplasms and IgE-dependent allergic reactions to food. Lastly, GI eosinophilia that is clearly aggressive, both because of its intensity and its persistence, is what characterizes eosinophilic gastroenteritis. In the present article, we summarize the ethiopathogenic and clinico-epidemiological features of this process, as well as its position within the field of immunopathologic food intolerance.

Eosinophilia↗

PubMed2003

Immunologic interaction between infiltrating eosinophils and T lymphocytes in murine spontaneous eosinophilic myocarditis.

BACKGROUND: Eosinophilic myocarditis often occurs spontaneously in DBA/2 mice. Relationships between infiltrating eosinophils (Eos), T lymphocytes and interleukin-5 (IL-5) in this disorder were investigated microscopically and immunohistochemically. METHODS: Hearts from male DBA/2 mice were studied from 5 to 10 weeks of age. Anti-CD4 and anti-CD8 antibodies were used. Infiltrating Eos, white blood cells (WBC), and CD4+ and CD8+ T cells were counted. Interactions were assessed with multiple regression and forward stepwise regression tests. Additionally, IL-5 distribution in heart tissue was histologically observed with special reference to immunological findings. RESULTS: Beginning at 5 weeks, several necrotic foci containing many damaged cardiocytes were seen in the epicardium of the right ventricle. Eos and lymphocytes were numerous within and around the necrotic foci. Eos were occasionally seen adjacent to degenerating cardiocytes. Three quarters of the mice exhibited such Eo-related myocardial damage. CD4+ lymphocytes were often seen infiltrating actively inflamed foci where Eos could also be observed. The lesional CD4+-to-CD8+ ratio (CD4/CD8) was 5.2 +/- 3.3 at 6 weeks, 6.8 +/- 3.7 at 7 weeks, and 1.5 +/- 0.8 at 10 weeks of age. The lesional Eo/WBC ratio was directly proportional to the CD4/CD8 ratio (p < 0.05), and was also significantly related to lesional CD4+ T cell count (p < 0.05). IL-5 was also expressed in Eo-rich areas. CONCLUSIONS: In this mouse strain with susceptibility to eosinophilic myocarditis, Eo infiltration was related to increased lesional CD4+ cell count. We suspect that CD4+ T cells induce local eosinotaxis, mediated by IL-5, and participate in myocardiocyte injury via Eo induction.

Animals↗

PubMed1978

Modulation of eosinophil chemotaxis and eosinophil chemotactic factor release by concanavalin A.

Concanavalin A (Con A) is not a chemotactic factor for guinea pig eosinophil leukocytes. It does, however, modulate the response of cells to neutrophil-derived eosinophil chemotactic factor (ECF) or to C5a. This effect occurs by a direct interaction of Con A with the target cell and is reversible by appropriate doses of alpha-methyl-D-mannoside (alpha-MM). The inhibition of chemotaxis at high doses of Con A is due to agglutination of the cells on top of the filter. The mechanism of enhancement at low doses is not understood, but several possible explanations are explored. Careful definition of the effect of Con A on eosinophil chemotaxis makes it possible to exclude an effect of Con A on ECF secretion by neutrophils.

Animals↗

PubMed1991

Characterization of eosinophils in a continuous ambulatory peritoneal dialysis patient with eosinophilic peritonitis.

A continuous ambulatory peritoneal dialysis patient developed eosinophilic peritonitis and was followed for 7 months. After 1 month, the peritonitis resolved, with a concomitant drop in percentage of hypodense eosinophils (Eos) recovered from peritoneal dialysate (PD) as well as a drop in fluid major basic protein levels. Blood eosinophil differential percentages were low, but the percentage of hypodense Eos in the blood tended to be relatively increased. Stool samples showed no evidence of parasitic infection, and epicutaneous skin tests were negative. Leukotriene C4 levels remained relatively constant as did white blood cell counts. Flow cytometric analysis of lymphocytes and granulocytes from PD and blood revealed high levels of CD23-positive lymphocytes.

Adult↗

PubMed1994

Incorporation of radioactive phosphate from adenosine triphosphate into phosphatidylinositol-4-phosphate in human peripheral blood hypodense eosinophils is less than in the normodense eosinophils.

Peripheral blood eosinophils from patients with atopic dermatitis and normal healthy controls were isolated on a Percoll gradient and incubated with [gamma 32P]ATP in the presence of Mg2+. After stopping the reaction, lipid extraction was performed with acidic medium and phospholipids were separated by thin-layer chromatography on 1% (w/v) oxalic acid-impregnated silica gel plates. In the autoradiographs considerable amounts of the radioactivity were found to be incorporated into phosphatidylinositol-4-phosphate. 32P incorporation into phosphatidylinositol-4-phosphate in hypodense eosinophils from atopic dermatitis patients was less than in normodense eosinophils from the same patients and controls.

Adenosine Triphosphate↗

PubMed1981

Selective inhibition of nonspecific eosinophil staining or identification of eosinophilic granulocytes by paired counterstaining in immunofluorescence studies.

Nonspecific staining of eosinophilic granulocytes produced by nonimmune rabbit IgG conjugates, highly labeled with fluorescein isothiocyanate (FITC) or tetramethylrhodamine isothiocyanate (MRITC), was efficiently inhibited by pretreatment of tissue sections with diaminobenzidine and hydrogen peroxide; the brown reaction product developed in the presence of this substrate by the endogenous peroxidase of the granulocytes sheltered these cells from subsequent nonspecific staining without interfering with specific immunofluorescence staining of other tissue elements. Similar results were obtained with the alternative noncarcinogenic peroxidase substrate, p-phenylenediamine-pyrocatechol. Alternatively, the eosinophils could be identified by their nonspecific staining with FITC-labeled bovine serum albumin when this conjugate was combined with an MRITC conjugate used for specific staining; optical conditions selective for green and red fluorescence discriminated distinctly between double-stained eosinophils and purely red specifically stained cells.

Coloring Agents↗

PubMed1985

Non allergic rhinitis: demography of eosinophils in nasal smear, blood total eosinophil counts and IgE levels.

Seventy-eight consecutive patients with non allergic rhinitis (negative allergy skin tests) were evaluated and classified as to possible causes using strict criteria. Sixty-one percent had vasomotor rhinitis (VMR), 33% had non allergic rhinitis with eosinophilia syndrome (NARES), 16% had sinusitis, 12% had a possible hidden allergy (elevated IgE), 4% had blood eosinophilic non allergic rhinitis (BENAR) and 2% had hypothyroidism. Some overlapping of diagnosis was present. Five per cent or greater eosinophils in the nasal smear appeared to be enough to consider the diagnosis of NARES. Sinusitis tended to be more significant in the NARES group compared to VMR. BENARS may be a new syndrome. It differs from NARES in that BENARS has markedly elevated blood eosinophilia and possibly no associated sinusitis. It is similar to NARES in that it has negative allergy skin test, normal serum IgE, and eosinophils in nasal secretions. Other causes of eosinophilia were excluded in our NARES and BENARS groups.

Adolescent↗

PubMed1999

Eosinophil activation in the tissue: synthetic steroid, budesonide, effectively inhibits the survival of eosinophils isolated from peripheral blood but not nasal polyp tissues.

We investigated the effect of a potent synthetic steroid, budesonide (BUD), on the survival of nasal polyp (NP) derived eosinophils (EOS). BUD, at the highest dose used, 10(-6) M, decreased this survival but only by approximately one third. We speculated that the relatively small inhibitory effect of budesonide on the survival of NP-EOS could be the result of these EOS being exposed to substantial amounts of GM-CSF, IL-5 or IL-3. In this regard, we detected 148 pg of GM-CSF per 150 mg of tissue, which approximately contained 106 of eosinophils, in the supernatant of NP explants for 24 h without any stimulation. Contents of both IL-5 and IL-3 were much less. We further studied survival of PB-EOS exposed to rhGM-CSF and found that 10(-6) M of BUD could only inhibit by less than one third the survival of PB-EOS exposed to an amount of rhGM-CSF, similar to that detected in the supernatant of NP explants. In addition, we exposed PB-EOS to 200 pg/ml of rhGM-CSF for a relatively long period of time (4 days) in order to mimic chronic exposure in the tissue and found that the survival of these cells was prolonged to the extent similar to that observed in NP-EOS. Our data suggests that the prolonged spontaneous survival of NP-EOS ex vivo is likely the result of sustained in vivo exposure to GM-CSF and budesonide has a smaller inhibitory effect in the survival of these eosinophils as compared to those from peripheral blood.

Administration, Topical↗

PubMed1975

Isochromosome 17 in a case of eosinophilic leukaemia. An abnormality common to eosinophilic and neutrophilic cells.

In a patient with eosinophilic leukaemia, serial chromosome studies using the Giemsa banding technique revealed a similar marker chromosome, identified as an isochromosome 17, in all bone marrow metaphases analysed. There was no Ph-1-chromosome. The cytogenetic data support the view that eosinophilic leukaemia is a specific disease entity, and suggest that both eosinophilic and neutrophilic cells are involved in the leukaemic process.

Bone Marrow Cells↗

PubMed1990

[Eosinophilic ulcer of the tongue. Pathogenic role of eosinophils].

A male patient with an ulcerative lesion on the edge of his tongue is present. The histopathologic findings were typical for "Eosinophilic Ulcer of the Tongue". This was contiguous with a carious molar, the remotion of which was followed by total remission of the ulcer. Its possible aetiology and pathogenesis are discussed. Based on the injurious effects of eosinophils mentioned in anothers affections the authors postulate that eosinophils may have an important rol in production or maintainance of this ulcer.

Aged↗

PubMed1978

Blood eosinophil leucocyte and eosinophil cationic protein. In vivo study of the influence of beta-2-adrenergic drugs and steroid medication.

The in vivo effect of beta-2-adrenergic stimulating and blocking drugs and of corticosteroid medication on blood eosinophils and serum eosinophil cationic protein (S-ECP) has been studied. The beta-2-adrenergic drugs, salbutamol and terbutaline, had an eosinopenic effect. They were able to decrease S-ECP concentration, which administration of steroid was not, indicating that only the adrenergic stimulators affect leucocyte secretion. Care must be taken in interpretation of blood eosinophil count and S-ECP concentration, and the actual medical treatment must be known.

Adrenal Cortex Hormones↗

PubMed1984

Surface proteins of the human eosinophil. I. Isolation of eosinophil IgG binding proteins.

Proteins involved in the attachment of eosinophils to immobilized antigen-antibody complexes were isolated. Eosinophils, purified from normal human peripheral blood, were surface labelled with 125I-iodide in the presence of lactoperoxidase and hydrogen peroxide. Immobilized immune complexes were prepared by covalent coupling of tetanus toxoid antigen to cellulose and treatment of the fixed antigen with human anti-tetanus IgG. Intact cells were allowed to interact with the antigen-antibody complex and the cells were then lysed in situ with a salt solution containing the non-ionic detergent NP40. After exhaustive washing to remove unattached proteins, the bound proteins were eluted with a buffer containing mercaptoethanol with or without SDS. A major protein of mol. wt 16K and a minor protein of mol. wt 18K were isolated. These proteins were unaffected by the temperature of attachment of eosinophils to the fixed IgG antigen complexes or by the presence of protease inhibitors and did not therefore appear to be proteolytic cleavage products.

Antigen-Antibody Complex↗