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At least 19 recordsLinked to original sources

PubMed1977

Chronic eosinophilic pneumonia. Ultrastructural evidence of marked immunoglobulin production plus macrophagic ingestion of eosinophils and eosinophilic lysosomes leading to intracytoplasmic Charcot-Leyden crystals.

A 60-year-old man was diagnosed as having chronic eosinophilic pneumonia by clinical presentation and open lung biopsy. Electron microscopic study of the tissue from biopsy revealed evidence of marked production of immunoglobulin, which may be part of the chemotactic process which attracted large numbers of eosinophils into the area. Also, there were macrophages which were phagocytosing degenerating eosinophils and eosinophilic lysosomes. Charcot-Leyden crystals were noted in the cytoplasm of many macrophages. The relationship of the production of immunoglobulin to the eosinophilia and the mechanism of intramacrophagic formation of Charcot-Leyden crystals is discussed.

Humans↗

PubMed1977

Antibody-dependent eosinophil-mediated damage to 51Cr-labeled schistosomula of Schistosoma mansoni: damage by purieid eosinophils.

After earlier observations that antibody-dependent, cell-mediated damage to 51Cr-labeled schistosomula can be ablated by pretreatment of a mixed preparation of human peripheral blood leukocytes with an anti-eosinophil serum and complement, we investigated the cytotoxic effects of eosinophil-enriched cell preparations. Preparations containing up to 98.5% eosinophils and devoid of neutrophils were effective in mediating antibody-dependent damage to schistosomula. Preparations enriched in mononuclear cells or in neutrophils, and devoid of eosinophils, were inactive. Eosinophils from some patients with eosinophilia induced by schistosomiasis were less active on a cell-to-cell basis than cells from normal individuals. The possibility that such cells were initially blocked by immune complexes was considered, and it was found that reasonable cytotoxicity by purified eosinophils from patients with eosinophilia could be generated by overnight cultures. A possible requirement for cooperation between eosinophils and other cell types was also studied. Lymphocytes, neutrophils and monocytes failed to enhance eosinophil-mediated cytotoxicity. These results provide further evidence that the eosinophil is the only cell in man responsible for antibody-dependent, complement-independent damage to schistosomula in vitro. Eosinophils from individuals, however, differ in their cytotoxic potential by a mechanism yet to be elucidated. The possible relationship of these findings to immunity in vivo is discussed.

Animals↗

PubMed1979

Interactions between human eosinophils and schistosomula of Schistosoma mansoni. II. The mechanism of irreversible eosinophil adherence.

Previous work (1)(1) has shown that normal human eosinophils show a preferential capacity, in comparison with neutrophils, to bind to antibody- coated schistosomula of Schistosoma mansoni. This effect is attributable to a temperature-dependent function of the eosinophil which renders its binding stable and irreversible by aggregated gamma globulin or Staphylococcus aureus protein A. In contrast, the binding of neutrophils is readily reversible by these agents. It has now been shown that the differences observed between eosinophils and neutrophils is a property of their interaction with living schistosomula. When dead or artificially damaged schistosomula were tested, neutrophils showed a markedly enhanced capacity to adhere, in both the presence and absence of anti-chistosomular serum. Subsequent experiments were designed to test the hypothesis that the strong, stable binding of eosinophils was attributable to degranulation, with release of granule contents which would then serve as ligands to bind the cell to the organism. First, an enhanced adherence both of eosinophils and of neutrophils could be demonstrated in the presence of eosinophil major basic protein (MBP) or of protamine, a high molecular weight cation. Second, the binding of eosinophils induced by concanavalin A (Con A) was found to differ markedly from that induced by antischistosomular serum. Con A-mediated binding of eosinophils was fully reversible by alpha-methyl-mannoside, was not associated with damage to the organism, and did not lead to degranulation of the cell, as estimated by measuring the release of MBP into the culture supernate. However, induction of degranulation of concanavalin A-bound eosinophils, but not of neutrophils, with the calcium ionophore A23187 converted the reaction into one which was no longer reversible by alpha- methylmannoside and in which damage to the organism now did occur. These findings support the hypothesis that the stable binding of eosinophils is associated with degranulation, a process which may contribute to the preferential capacity of this cell to mediate antibody-dependent damage to schistosomula.

Antibodies↗

PubMed1975

Behavior of eosinophil leukocytes in acute inflammation. II. Eosinophil dynamics during acute inflammation.

The marked diminution in the number of circulating eosinophils, which has been shown to occur during acute bacterial infections, is a distinctive aspect of eosinophil physiology and of the host response to acute infection. The mouse rendered eosinophilic by infection with trichinosis provides a suitable model for study of the eosinopenic response induced by acute inflammation. The alterations in eosinophil dynamics associated with acute inflammatory reactions in trichinous mice were studied with pneumococcal abscesses, with Escherichia coli pyelonephritis, with Coxsackie viral pancreatitis, and with acute subcutaneous inflammation due to turpentine. Each of these stimuli of acute inflammation markedly suppressed the eosinophilia of trichinosis. This suggests that the eosinopenia is a response to the acute inflammatory process rather than the response to a specific type of pathogen. These studies apply quantitative techniques to ascertain the effects of acute inflammation on eosinophil production in bone marrow and on distribution of eosinophils in the peripheral tissues. From these observations, it is apparent that the initial response to acute inflammation includes a rapid drop in numbers of circulating eosinophils, a rapid accumulation of eosinophils at the periphery of the inflammatory site, and an inhibition of egress of eosinophils from the bone marrow. With prolongation of the inflammatory process, inhibition of eosinopoiesis occurs.

Acute Disease↗

PubMed1979

Unique characteristics of superoxide production by human eosinophils in eosinophilic states.

Eosinophils from patients with peripheral blood eosinophilia and human neutrophils from normal subjects and patients with neutrophilia produced superoxide anion (O2-) in vitro at similar rates in the absence of stimulation and exhibited comparably increased rates of O2- production during the initial 1 h of incubation with opsonized zymosan. In the presence of opsonized zymosan, the rate of O2- production by eosinophils was constantly high for 3 h, whereas the rate of production by neutrophils fell by more than 65% after 1 h. Consequently, the amount of superoxide produced by phagocytizing leukocytes was twofold higher for eosinophils than for neutrophils at 3 h. O2- production by cell-free sonicates of zymosan-stimulated eosinophils and neutrophils exhibited the same preference for NADPH over NADH. One mM sodium azide significantly decreased the generation of O2- by phagocytizing eosinophils, but lacked an effect on neutrophils. the prolonged release of O2- by eosinophils engaged in phagocytosis may contribute both to their unique microbicidal profile and to the capacity of eosinophils to injure host tissues in some eosinophilic syndromes.

Eosinophilia↗

PubMed1977

Reactive eosinophilic pleuritis: a lesion to be distinguished from pulmonary eosinophilic granuloma.

Pleural nodules or sheets of histiocytes, admixed with eosinophils, giant cells, and other inflammatory cells are observed frequently in patients with spontaneous pneumothorax. This reaction, designated reactive eosinophillic pleuritis (REP), can closely resemble eosinophilic granuloma. Reactive eosinophilic pleuritis was found in pleural tissue of 22 of 57 patients with spontaneous pneumothorax in whom tissue was available for study. None of these patients had clinical or radiographic evidence of interstitial lung disease. Follow-up of 20 patients with REP ranged from six months to five years. None developed evidence of eosinophilic granuloma. Electron microscopy of one case did not show the Langerhans granules characteristic of the histiocytoses, including eosinophilic granuloma. Reactive eosinophilic pleuritit appears to be a nonspecific reaction to pleural injury, and is not a prodromal feature of pulmonary eosinophilic granuloma.

Diagnosis, Differential↗

PubMed1978

Anisakis and eosinophil. I. Detection of a soluble factor selectively chemotactic for eosinophils in the extract from Anisakis larvae.

Studies were undertaken in order to determine if Anisakis larva itself has the ability to attract eosinophils. Extracts from Anisakis larvae were examined for both neutrophil and eosinophil chemotactic activities with both in vivo and in vitro assay systems. When the soluble extract was injected intradermally into normal guinea pigs, a profound accumulation of eosinophils was observed at the injection site. The cells started to accumulate at the site within 1 hr and the number of eosinophils at the site reached its peak at 8 hr after the injection of the extract. Such eosinophilic accumulation was enhanced in a dose-response fashion over the range of 0.5 to 50 micrograms protein. The strong chemotatic activity of the Anisakis extract for eosinophils was confirmed when in vitro chemotaxis assays were performed with Boyden chemotatic chambers. Interestingly, no chemotactic activity for neutrophils was found at those concentrations of the extract with which the eosinophil effect was observed. These results indicate that the factor described here, in addition to the various known immunologic factors, may play an important role in the development of eosinophilia in anisakiasis.

Animals↗

PubMed1976

Structural determinants of the eosinophil: chemotactic activity of the acidic tetrapeptides of eosinophil chemotactic factor of anaphylaxis.

The acidic tetrapeptides of ECF-A, Ala/Val-Gly-Ser-Glu, exhibit peak in vitro chemotactic activity for human eosinophils at concentrations of 3 X 10(-8) M to 10(-6) M, and rapidly deactivate eosinophils to homologous and other stimuli at concentrations as low as 10(-10) M. The analogue Leu-Gly-Ser-Glu reaches peak activity at 10(-8)M-10(-7)M, while Phe-Gly-Ser-Glu requires 10(-4)M to elicit a peak response. Although inversion of the order of glycine and serine does not alter the eosinophil chemotactic activity of the tetrapeptides, deletion of glycine increases by 10-fold the concentration required for peak chemotactic activity, indicating the critical nature of the spacing between NH2- and COOH-terminal residues. The substituent COOH-terminal tripeptide, which is only marginally chemotactic, irreversibly suppresses eosinophil chemotactic responsiveness at a concentration 10,000-fold higher than concentrations necessary for deactivation by the intact tetrapeptide. The high concentration of tripeptide required for this cell directed effect, which is assumed to be analogous to deactivation, is attributed to the absence of the NH2-terminal residue which would facilitate effective interaction with the eosinophil. A substituent NH2-terminal tripeptide and amides of the NH2-terminal amino acids, which are devoid of chemotactic and deactivating activities, reversibly inhibit the tetrapeptide stimulus in a dose-response fashion. The additional finding that the NH2-terminal tripeptide protects the eosinophil from deactivation by the intact tetrapeptide confirms that the competitive interaction is stimulus specific.

Alanine↗

PubMed1977

Different composition of the eosinophilic bone marrow pool in reactive eosinophilia and eosinophilic leukaemia.

The composition of the eosinophilic cell series in the bone marrow has been analysed in 10 patients with a pronounced reactive eosinophilia (RE) and in 2 with eosinophilic leukaemia (EL). An imparied differentiation of the eosinophils was found in the EL patients compared with the RE group. Thus the ratio of eosinophilic promyelocytestmyelocytes: segmented eosinophils was 9.2 and 9.1, respectively, in the patients with EL and 0.1--3.1 (average 1.3) in the RE patients. It is suggested that EL is characterized by an impaired differentiation of the eosinophilic bone marrow cells and that the recognition of this abnormality is of value in the diffential diagnosis between EL and RE.

Adult↗

PubMed1979

Blood eosinophils and eosinophil cationic protein after acute myocardial infarction or corticosteroid administration.

Measurements of eosinophil cationic protein in serum (S-ECP) have been made in patients with acute myocardial infarction. In spite of low numbers of blood eosinophils in the acute phase of the disease S-ECP levels fluctuated widely with often markedly raised levels. Peak levels of S-ECP were significantly correlated (P less than 0.001) to peak numbers of blood eosinophils, although the former usually occurred within the first 2-3 d of illness and the latter usually after the sixth day. Intravenous injection of 0.5 g methylprednisolone in healthy individuals reduced blood eosinophil counts for at least 24 h, but S-ECP levels remained within normal limits. These results suggest that ECP is released from eosinophils in vivo. The raised levels of S-ECP in patients with acute myocardial infarction are probably due to the active participation of eosinophils in the inflammatory process.

Acute Disease↗

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↗

PubMed1978

High resolution autoradiographic studies of RNA, protein and DNA synthesis during human eosinophil granulocytopoiesis: evidence for the presence of RNA on or within eosinophil granules.

Human bone marrow cells which had been incubated with [3H]uridine or [3H]leucine for I h were studied using the technique of electron microscope-autoradiography. The autoradiographs revealed the presence of newly-synthesized RNA and protein molecules within or on a proportion of (I) the primary and secondary granules in all classes of eosinophil precursors and (2) the secondary granules in eosinophil granulocytes. It is suggested that the granule-associated RNA molecules may be concerned with the synthesis of at least some of the new protein molecules which were incorporated into the limiting membrane or substance of eosinophil granules long after the immature primary granule stage. Studies of eosinophil precursors which had been incubated with [3H]thymidine for I h showed that the eosinophil granules do not label with this DNA precursor.

Autoradiography↗

PubMed1975

Chemotactic deactivation of human eosinophils by the eosinophil chemotactic factor of anaphylaxis (38527).

Purified human eosinophils demonstrate diminished chemotactic responsiveness (deactivation) after incubation with the eosinophil chemotactic factor of anaphylaxis (ECF-A). The deactivation is rapid and selective in that ECF-A deactivated human eosinophils more markedly than neutrophilic or mononuclear leukocytes. The eosinophil can also be deactivated by C5a which is eosinophilotactic, and there is cross deactivation between C5a and ECF-A. Deactivation may be an important physiologic control mechanism enabling the eosinophil to remain at sites of ECF-A release in order to manifest its regulatory functions in immediate hypersensitivity reactions.

Anaphylaxis↗

PubMed1977

Arginine-rich cationic proteins of human eosinophil granules: comparison of the constituents of eosinophilic and neutrophilic leukocytes.

Several arginine-rich cationic proteins previously isolated from granules of leukemic myeloid cells have been found to reside primarily in human eosinophil leukocytes. The major component has a molecular weight of 21,000 and it contains approximately 2.6 moles of zinc per mole of protein. Velocity centrifugation of cytoplasm from leukocytes of patients with marked eosinophilia showed that this group of proteins is packaged in the crystalloid-containing large eosinophil granules. Approximately 30% of the protein content of eosinophil granules belonged to this group of cationic proteins. Bactericidal or esterolytic activities of the cationic proteins were not detected, nor did they inhibit guinea pig anaphylatoxin or histamine-induced contraction. The basic protein previously demonstrated in guinea pig eosinophils may be analogous to the group of basic proteins of human eosinophils but great differences are found for molecular weight and amino acid composition.

Acid Phosphatase↗

PubMed1975

Role of the eosinophil in the allergic reactions. I. EDI-an eosinophil-derived inhibitor of histamine release.

An inhibitor of histamine release was found to be associated with the human eosinophilic leukocyte. This eosinophil-derived inhibitor (EDI) was released from eosinophil-rich fractions upon sonication or interaction with immune reactants (specific allergens or anti-IgE). EDI was found to exert its inhibitory action at the target cell level by increasing the intracellular levels of cyclic-AMP. Preliminary electron microscopic studies show the presence of IgE on the eosinophilic leukocyte and it is suggested that the allergen or anti-IgE-induced release of EDI might be due to a direct interaction of these immune reactants with the eosinophil-bound IgE antibody. The results also suggest that by virtue of liberating a histamine release inhibitor such as EDI, the eopsinophil assumes a modulating role in the allergic inflammatory reaction.

Animals↗

PubMed1975

Role of the eosinophil in the allergic reactions. II. Release of prostaglandins from human eosinophilic leukocytes.

Human eosinophilic leukocytes respond to a variety of stimuli by liberating an inhibitor of histamine release. The active principle(s) in this eosinophil-derived inhibitor (EDI) was found to be a mixture of acidic lipids of similar physiocochemical behavior and biologic activity to prostaglandins E1 and E2. Indomethacin, an inhibitor or prostaglandin synthesis, specifically blocked the immune release of EDI. The results indicate that stimulation of human eosinophilic leukocytes results in synthesis and release of prostaglandins E1 and E2 from these cells. These findings strongly support the hypothesis that the eosinophil assumes a modulatory role in the allergic inflammatory reaction. The ways by which, under specific antigenic (allergenic) stimulation, human eosinophils could modulate the events asssociated with the allergic response, through the released prostaglandins, are discussed.

Adenosine Diphosphate↗

PubMed1978

Rat mast cell-eosinophil interaction in antibody-dependent eosinophil cytotoxicity to Schistosoma mansoni schistosomula.

The involvement of IgG2a antibodies and mast cells in antibody-dependent eosinophil cytotoxicity suggested a possible interaction between mast cells and eosinophils for in vitro killing of Schistosoma mansoni schistosomula. Cell purification procedures showed that a minimum ratio of mast cells was required to obtain eosinophil cytotoxicity. The incubation of mast cells with heat-aggregated IgG2a immunoglobulins before addition to a mast cell-depleted eosinophil population induced a significant degree of inhibition of cytotoxicity, Similarly, the heat-aggregated IgG2a Fc fragment had a strong inhibitory effect whereas incubation of mast cells with Fab fragment failed to inhibit the cytotoxic effect. The Fc portion of IgG2a immunoglobulins therefore seemed to be involved in binding to the mast cell surface. Furthermore, it was demonstrated that soluble mediators released after mast cell activation either by compound 48/80, or by IgE, or IgG2a-dependent reaction had the same effect as intact mast cells. These observations suggest that the eosinophil-dependent cytotoxicity mechanism requires a signal provided by soluble mast cell mediators in addition to antibody.

Animals↗

PubMed1979

Comparison of the ability of eosinophils and neutrophils, and of eosinophils from patients with S. mansoni infection and normal individuals, to mediate in vitro damage to schistosomula of S. mansoni.

A reliable and reproducible method that produces separate fractions of pure eosinophils and neutrophils from normal peripheral blood was described. The interaction of eosinophils and neutrophils with antibody coated schistosomula was examined in vitro. Neutrophils were highly active in the 51Cr release assay and most formed rosettes with antibody coated red cells, but they adhered poorly to schistosomula and did not kill the organisms. Eosinophils, although they were less active in the 51Cr release assay than neutrophils and few formed rosettes, adhered strongly to schistosomula and, in the presence of antibody, were able to kill organisms. Organisms from patients with S. mansoni infection and eosinophilia were more effecient than eosinophils from normal individuals in their capacity to release 51Cr from labelled somula in the presence of antibody.

Antibodies↗