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PubMed1990

Mechanisms of eosinophil accumulation around eggs of Schistosoma japonicum: role of two purified components, allergen and eosinophil chemotactic factor, from soluble egg antigens measured on sensitized guinea pig skin.

Mechanisms of eosinophil response induced by soluble egg antigen (SEA) in Schistosoma japonicum-infected guinea pig tissues were analyzed using two purified components of SEA: major allergenic components (JEAL) and a major eosinophil chemotactic component (ECF-SjE). Eosinophil response to the crude SEA of S. japonicum was detected at the injection site mainly at 2-8 h after the antigenic challenge; this response consisted of two different phases of eosinophil attraction. An early phase (2 h) was mediated by an immediate-type hypersensitivity reaction; JEAL played an important role in mediating this phase of eosinophil response. A late phase (8 h) was mediated by ECF-SjE. Therefore, this phase of eosinophil response was caused by direct eosinophilotactic activity of SEA. These two types of eosinophil response must be important processes in the formation of S. japonicum egg-associated eosinophilic granuloma.

Allergens↗
PubMed1990

Effect of eosinophil-degranulating estrogens on spleen eosinophils and white pulp/red pulp ratio.

A role for eosinophils in the immune reaction has not been yet established. Considering that these leukocytes accumulate in lymphoid organs under glucocorticoid stimulation, we explored the possibility that they participate in the depression of immune reactions induced by these hormones and that they degranulate to exert this action. In this context, we investigated the dose effect of three estrogens on the number and degranulation of spleen red pulp eosinophils and on the percentage of spleen cross sectional area comprising white pulp. Estradiol-17 beta or 4 (OH) estradiol-17 beta increased red pulp eosinophils at low doses: 2 (OH) estradiol-17 beta increased them at a very high dose. The three estrogens degranulated the spleen eosinophils and decreased the lymphocyte containing spleen white pulp. We propose that the decrease in white pulp is a response mediated by agents released from degranulating eosinophils under the action of estrogen. Consequently, both estrogen-induced eosinophil degranulation and estrogen-induced increase in red pulp eosinophil numbers are conditions contributing to a decrease in white pulp volume. All above evidence supports the hypothesis that eosinophils are involved in immunoregulation by diminishing the number of lymphocytes contained in lymphoid organs.

Animals↗
PubMed2003

Changes in the peripheral eosinophil count in patients with acute eosinophilic myocarditis.

In many cases, the diagnosis of eosinophilic myocarditis is suggested by an elevated peripheral blood eosinophil count. However, no detailed studies have been performed on the sequential changes in the initial peripheral blood eosinophil count over the course of the disease. We measured the peripheral blood eosinophil count at the time of presentation in eight patients with eosinophilic myocarditis proven by endomyocardial biopsy and intermittently thereafter. The eosinophil count at the time of onset was <500/mm(3) in four patients, >500/mm(3) but <1,000/mm(3) in three patients, and > or =1,000/mm(3) in one patient. In three of the four patients with an initial eosinophil count of <500/mm(3), an increase to > or =500/mm(3) occurred 7-12 days after the onset. The remaining patient did not develop peripheral eosinophilia. In conclusion, in the early stage of eosinophilic myocarditis, peripheral hypereosinophilia is not present initially in some patients, and may not develop during the course of the illness in a subset of these patients.

Acute Disease↗
PubMed2004

The pathobiology of eosinophilic gastroenteritis of childhood: is it really the eosinophil, allergic mediated, or something else?

Over the past decade clinicians have witnessed a dramatic rise in the prevalence of eosinophilic gastrointestinal diseases. Diverse symptoms, a broad range of endoscopic findings, and varying histopathologic features pose several questions: Do eosinophils represent an allergic response? What mechanisms drive eosinophils to specific mucosal targets? How do eosinophils affect the gastrointestinal tissues? Recent clinical and basic studies are investigating the pathogenesis of eosinophilic gastrointestinal diseases. This review highlights the literature concerning the mechanisms that govern these diseases, with a specific focus on diseases of gastrointestinal columnar epithelia (eosinophilic gastroenteritis and eosinophilic colitis). The roles of specific chemokines, such as eotaxin, and the data supporting the involvement of eosinophil granule proteins in disease states, are discussed.

Animals↗
PubMed1990

A new method for measuring eosinophil activating factors, based on the increased expression of CR3 alpha chain (CD11b) on the surface of activated eosinophils.

The observation that activation of eosinophils in vitro with PAF increases the surface expression of the alpha chain of the complement receptor CR3 (CD11b) has been extended to other eosinophil activating factors. CD11b may be detected on activated eosinophils by reaction with mouse monoclonal anti-human CD11b IgG, following the addition of urease-conjugated sheep anti-mouse IgG. CD11b levels were increased on eosinophils after incubation with (a) recombinant colony stimulating factors, IL-3, GM-CSF and IL-5, at concentrations of 100 U/ml, or (b) with eosinophil activating factors, recombinant TNF alpha (1000 U/ml), EAF purified from mononuclear cell supernatants and PAF (10(-6) M). CD11b levels were not affected by IL-1 alpha, IL-2 or IFN-gamma. Unstimulated neutrophils had higher levels of CD11b than unstimulated eosinophils, but neutrophil CD11b was unaffected by IL-3, GM-CSF and IL-5 and was only slightly affected by TNF, EAF and PAF. Polyclonal rabbit antibodies to IL-3 and TNF neutralised their CD11b enhancing activities. The PAF antagonists WEB 2086 and WEB 2170 neutralised the CD11b enhancing activity of PAF. We conclude that measurement of CD11b expression on eosinophils is a convenient method for the assay of eosinophil activating activity.

Animals↗
PubMed1993

Eosinophil survival activity identified as interleukin-5 is associated with eosinophil recruitment and degranulation and lung injury twenty-four hours after segmental antigen lung challenge.

BACKGROUND: Segmental antigen challenge in allergic volunteer subjects leads to the recruitment of inflammatory cells, including eosinophils, to the lung and to lung injury as shown by albumin influx into the alveolar air space. The goal of this study was to determine whether eosinophil-active cytokines, including IL-3, IL-5, or granulocyte-macrophage colony-stimulating factor, are released into the lung 24 hours after segmental antigen challenge of ragweed allergic subjects with allergic rhinitis and to determine whether the presence of the cytokine or cytokines is correlated with markers of lung inflammation and lung injury. METHODS: Volunteers underwent challenge with a wide variety of antigen doses, which resulted in the recruitment of inflammatory cell mixtures both with and without eosinophils. RESULTS: Eosinophil survival activity (ESA), the ability of the cytokine to prolong blood eosinophil survival in culture, was found in 5 of 17 ragweed allergic subjects and only in subjects challenged with relatively high doses of ragweed antigen (0.2 ragweed antigen units/ml or more). No ESA was found in bronchoalveolar lavage (BAL) fluid in any of eight nonragweed allergic subjects. This activity could be almost completely neutralized by preincubating BAL fluid with specific antibody to IL-5, although a small contribution by granulocyte-macrophage colony-stimulating factor may also have been present. ESA correlated with eosinophil recruitment (r = 0.72, p < 0.001) and degranulation in the lung (r = 0.63 to 0.81, p < 0.01, for eosinophil granule constituents in BAL fluid) and lung injury as shown by albumin influx into the alveolar air spaces (r = 0.83, p < 0.001). ESA was unrelated to the presence of other inflammatory cells in the lung. Subjects who had IL-5 in BAL fluid appeared to undergo more severe initial reactions to antigen challenge. CONCLUSIONS: We conclude that IL-5 is the most important constituent in ESA in the lung 24 hours after antigen challenge and that it correlates with eosinophil recruitment, degranulation, and lung injury.

Allergens↗
PubMed1995

Synergism of IL-3, IL-5, and GM-CSF on eosinophil differentiation and its application for an assay of murine IL-5 as an eosinophil differentiation factor.

In order to elucidate the mechanisms of eosinophil differentiation, we examined the effects of combinations of interleukin 5 (IL-5) with IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF) on in vitro differentiation into eosinophils from bone marrow cells of ICR mice. When the amount of added IL-5 was kept constant, IL-3 exhibited dose-dependent production of eosinophils both in the absence and presence of low doses of GM-CSF. In contrast, IL-5 plus GM-CSF showed highly enhanced production of eosinophils, and eosinophil production maximized at a concentration between 10 and 20 U/ml and decreased at higher concentrations. When IL-3 and GM-CSF were kept constant at concentrations of 20 U/ml and 10 U/ml, respectively, the number of eosinophils increased linearly in IL-5-dependent manner in a range from 0.3 to 30 U/ml. These results suggest that IL-3 and GM-CSF act synergistically with IL-5 in in vitro eosinophil differentiation. In addition, we propose a new method for quantifying eosinophil differentiation activity of IL-5.

Animals↗
PubMed2000

Hydrogen peroxide release from human eosinophils on fibronectin: scopoletin enhances eosinophil activation.

We have examined the release of H(2)O(2) from PAF or TNFalpha-stimulated human eosinophils on fibronectin (FN)-coated polystyrene plates. H(2)O(2) release was measured by the standard scopoletin-horseradish peroxidase (SCOP-HRP) method and compared with that measured by a new microplate fluorescent assay for H(2)O(2) using a novel HRP substrate A6550. We observed that the SCOP-HRP method gave a 25-fold higher estimate of H(2)O(2) release from eosinophils than did the A6550-HRP method. Microscopic examination of PAF or TNFalpha-stimulated eosinophils in buffer alone or A6550-HRP reaction mixture showed that the cells remained generally round, while eosinophils in SCOP-HRP reaction mixture were spread on the fibronectin-coated surface. Measurement of the cellular ATP content after PAF-stimulation showed that only eosinophils activated in SCOP-HRP had a 50% fall in ATP content. This supported our conclusion that measurement of H(2)O(2) release from eosinophils in SCOP-HRP reaction mixture is problematic since the SCOP-HRP system activates eosinophils. However, we also found that A6550-HRP, when present throughout the incubation, resulted in a lower estimate of H(2)O(2) release than expected. The method used to detect eosinophil H(2)O(2) release greatly influences the absolute amount of H(2)O(2) detected.

Adenosine Triphosphate↗
PubMed1983

Hydrogen peroxide release from eosinophils: quantitative, comparative studies of human and guinea pig eosinophils.

Eosinophils play an important role in host defense against parasitic infection, employing both oxidative and nonoxidative systems to effect damage. The active oxygen product, hydrogen peroxide, either alone or in combination with the enzyme eosinophil peroxidase, may damage parasites. These studies use a sensitive fluorometric assay to document the release of hydrogen peroxide from guinea pig peritoneal exudate eosinophils and human peripheral blood eosinophils. Guinea pig eosinophils released 0.13 +/- 0.02 (n = 10) nmol H2O2/10(5) eos/5 min under resting conditions which were markedly increased when stimulated by phorbal myristate acetate (PMA, 1 microgram/ml) [4.80 +/- 0.50 (19) nmol H2O2/10(5) eos/5 min], preopsonized zymosan [2.40 +/- 0.17 (4) nmol H2O2/10(5) eos/5 min], or latex beads [1.14 +/- 0.26 (5) nmol H2O2/10(5) eos/5 min]. Normal human peripheral blood eosinophils had greater resting release of hydrogen peroxide [0.34 +/- 0.05 (8) nmol H2O2/10(5) eos/5 min], but were less effectively stimulated by PMA [3.12 +/- 0.57 (9) nmol H2O2/10(5) eos/5 min], preopsonized zymosan [0.78 +/- 0.16 (8) nmol H2O2/10(5) eos/5 min] or latex beads [0.69 +/- 0.32 (6) nmol H2O2/10(5) eos] (p less than or equal to 0.05). Hydrogen peroxide release was markedly enhanced by the presence of exogenous glucose and was linearly dependent upon cell number when the soluble stimulus PMA was used. Particle-stimulated hydrogen peroxide was not necessarily enhanced by increases in the particle:cell ratio. The demonstration of the release of large amounts of hydrogen peroxide from eosinophils is further support for the concept that eosinophils play an active role in host defense.

Animals↗
PubMed2005

Viscum album agglutinin-I induces apoptosis and degradation of cytoskeletal proteins via caspases in human leukaemia eosinophil AML14.3D10 cells: differences with purified human eosinophils.

Although there are several agents that induce neutrophil apoptosis, few are known as inducers of eosinophil apoptosis. As eosinophils are potent effector cells contributing to allergic inflammation and asthma, we investigated whether the pro-apoptotic agent Viscum album agglutinin-I (VAA-I) could induce eosinophil apoptosis. VAA-I was found to induce apoptosis in eosinophilic AML14.3D10 (3D10) cells and that these cells expressed caspases-1, -2, -3, -4, -7, -8, -9 and -10. VAA-I-induced gelsolin degradation was reversed by the pan-caspase inhibitor N-benzyloxycarbonyl-V-A-D-O-methylfluoromethyl ketone (z-VAD). Also, paxillin, vimentin and lamin B1 were cleaved by caspases in VAA-I-induced 3D10 cells. VAA-I activated caspase-3 and -8 in 3D10 cells but, unlike z-VAD, treatment with a caspase-8 inhibitor slightly reversed apoptosis. Treatment of purified human eosinophils with VAA-I was found to induce apoptosis, degradation of gelsolin and lamin B1, but unlike 3D10 cells, cleavage of lamin B1 and cell apoptosis was not reversed by z-VAD. We conclude that VAA-I is a potent inducer of eosinophil apoptosis and that proteases other than those inhibited by z-VAD in 3D10 cells are involved in VAA-I-induced peripheral blood eosinophil apoptosis and lamin B1 cleavage. Thus, VAA-I represents a potential candidate for the reduction of the number of eosinophils in diseases where they play important roles.

Acute Disease↗
PubMed1993

The role of eosinophils in the pathogenesis of atopic dermatitis--eosinophil granule proteins as markers of disease activity.

Currently, there is a large body of evidence that atopic dermatitis (AD) has an immunologic basis. Atopy-specific helper T cells (Th2-like T cells) may play a pathogenetic role by producing and releasing cytokines relevant for the allergic inflammation, such as IL-4, IL-5, and other growth factors. Eosinophils are believed to be of major importance as effector cells mediating the pathogenetically relevant late-phase reaction which is associated with a significant destruction of the surrounding tissue. Accordingly, a significant preactivation of peripheral blood eosinophils was detected in AD patients, leading to an enhanced susceptibility of these cells to distinct stimuli such as IL-5. Toxic proteins, such as eosinophil cationic protein (ECP), contained in the matrix and the core of secondary granules of eosinophils, may play an important role by propagating the allergic inflammatory process and by modulating the immune response. The pathogenetic role of eosinophils in AD is further supported by the detection of these proteins in the eczematous skin of patients. Furthermore, recent data point to a significant correlation between disease activity and deposition of eosinophil granule content: ECP serum levels were significantly increased in AD patients. In addition, ECP levels correlated with the disease activity. Moreover, clinical improvement was associated with a decrease of both the clinical score and serum ECP levels. These data clearly indicate that activated eosinophils may play a major role in the allergic inflammatory process of AD. Therefore, modulation of eosinophil activation could prove to be an important pharmacologic modality for the treatment of AD.

Cytokines↗
PubMedDate not supplied

Eosinophil development and bone marrow and tissue eosinophils in atopic asthma.

BACKGROUND: Eosinophils develop from bone marrow (BM) progenitors, and interleukin-5 (IL-5) and eotaxin may act in expansion and mobilisation of BM eosinophils in asthma. METHODS: We have examined phenotypic changes as CD34+ cells develop to the eosinophil lineage in vitro, and have evaluated BM eosinophils from asthmatic and control subjects for expression of the eotaxin receptor, CCR3. RESULTS: Acquisition of receptors for IL-5 and CCR3 was an early event in eosinophil development. There were increased CD34+ cells, and mature and immature CCR3+ eosinophils in BM from asthmatics. CONCLUSION: These data suggest that IL-5 may act early in eosinophil development, and that eotaxin has the capacity to mobilise a BM eosinophil pool in asthma.

Antigens, CD34↗
PubMed2002

Hydrogen peroxide reverses IL-5 afforded eosinophil survival and promotes constitutive human eosinophil apoptosis.

BACKGROUND: Eosinophils play a central role in the induction and perpetuation of allergic inflammatory responses. The present study was performed to investigate the effects of reactive oxygen intermediates on constitutive apoptosis as well as on interleukin (IL)-5 afforded human eosinophil survival. METHODS: Peripheral blood eosinophils were isolated by CD16-negative selection to >99% purity and were cultured for 48 h. The number of apoptotic eosinophils in the culture was assessed by flow cytometric analysis of relative DNA content in propidium-iodide-stained cells, annexin-V binding or by morphological analysis. Apoptosis was confirmed by the appearance of a typical ladder pattern in the DNA fragmentation assay by agarose gel electrophoresis. RESULTS: Exogenous H(2)O(2) reversed IL-5-afforded eosinophil survival by inducing apoptosis. Constitutive eosinophil apoptosis was inhibited by a reduction of intracellular levels of H(2)O(2) by catalase. Exogenous H(2)O(2) increased the rate of constitutive apoptosis. CONCLUSIONS: Our results suggest that H(2)O(2) may play a role in the downregulation of eosinophilic inflammation by inducing eosinophil apoptosis.

Apoptosis↗
PubMed2005

NR4A orphan nuclear receptor family in peripheral blood eosinophils from patients with atopic dermatitis and apoptotic eosinophils in vitro.

To identify novel genes related to the clinical signs of atopic dermatitis (AD), differentially expressed genes were sought in peripheral blood eosinophils from both AD patients and healthy volunteers. RNA was prepared from eosinophils, expression of various genes was monitored using the Affymetrix GeneChip, and expression was quantified by real-time RT-PCR. Two genes, Nur77 and NOR1, members of NR4A orphan nuclear receptor family, were expressed at a significantly higher level in AD patients than in healthy volunteers. Expression of another gene in the NR4A receptor family, Nurr1, was also higher in AD patients than in healthy volunteers. When peripheral blood leukocytes from healthy volunteers were fractionated, NOR1 expression was highest in eosinophils, but expression of Nur77 and Nurr1 genes was not eosinophil-specific. Extremely intense apoptosis was induced in both eosinophils and an eosinophil cell line, AML14.3D10, by treatment with antibody (Ab) to both CD30 and Fas. Rapid expression of the genes for the NR4A receptor family was observed with anti-CD30 Ab treatment but not with anti-Fas Ab. The NR4A orphan nuclear receptor family gene expression and the subsequent eosinophil apoptosis were downregulated by the MAPK inhibitor, U0126. These results suggest that the expression of the NR4A receptor family genes through CD30 signaling may regulate eosinophil apoptosis in allergic conditions such as AD.

Adolescent↗
PubMed2005

Accumulation of CXCR3-expressing eosinophils and increased concentration of its ligands (IP10 and Mig) in bronchoalveolar lavage fluid of patients with chronic eosinophilic pneumonia.

BACKGROUND: Since human peripheral eosinophils have been shown to migrate to the CXC chemokine receptor 3 (CXCR3) ligands IFN-gamma-inducible protein 10 (IP10) and monokine induced by IFN-gamma (Mig), this confirms that CXCR3 is functionally expressed on these cells. IP10 expression has been shown to be increased in the airways of asthmatics. Eosinophil accumulations are found in bronchoalveolar lavage fluid (BALF) from patients with chronic eosinophilic pneumonia (CEP). To examine the contribution of IP10 and Mig in the pathogenesis of CEP, we measured the concentration of IP10 and Mig, and evaluated the expression of CXCR3 on eosinophils in BALF taken from patients with CEP. METHODS: The concentrations of IP10 and Mig in BALF were measured by ELISA. The proportion of CXCR3-expressing CD4+ T cells and CD16-negative eosinophils was determined by flow cytometry. RESULTS: The BALF concentrations of IP10 and Mig were higher in patients with CEP, as well as in patients with sarcoidosis, when compared to healthy controls. The absolute number of CXCR3+ CD4+ T cells was significantly higher in the BALF of patients with sarcoidosis, but not in the patients with CEP, when compared to healthy volunteers. There were higher percentages of CXCR3-expressing eosinophils in the BALF than in the peripheral blood of patients with CEP. CONCLUSIONS: Our findings suggest that IP10 and Mig contribute to the accumulation of CXCR3-expressing eosinophils in the lungs of patients with CEP, and modulate the eosinophilic inflammation of the lung.

Adult↗
PubMed1999

5-Oxo-6,8,11,14-eicosatetraenoic acid induces important eosinophil transmigration through basement membrane components: comparison of normal and asthmatic eosinophils.

Basement membrane transmigration is an important step in tissue recruitment of eosinophils into inflamed tissue. Recent reports showed that this phenomenon is modulated by platelet-activating factor (PAF) in combination with cytokines and proteinases. We investigated the in vitro efficacy of 5-oxo-6,8,11, 14-eicosatetraenoic acid (5-oxo-ETE), a metabolite of arachidonic acid and known as a potent eosinophil chemotactic factor, in promoting the transmigration of blood eosinophils from normal and asthmatic subjects through a Matrigel basement membrane. 5-Oxo-ETE proved to be a more potent (> 10-fold) inducer of eosinophil transmigration than PAF, and this effect was similar in cells from normal and asthmatic subjects (82.0 +/- 3.7% and 88.1 +/- 3.7%, respectively). Moreover, 5-oxo-ETE was active in the absence of interleukin (IL)-5, although this cytokine amplified the effect of 5-oxo-ETE from 61.3 +/- 3.3% to 92.8 +/- 1.8% (p = 0.003). The membrane receptor for urokinase plasminogen activator (CD87), a serine protease, was observed on eosinophils, and its expression was increased by IL-5. The inhibition of both metalloproteinases (MMP) and plasmin/plasminogen complex with inhibitor or monoclonal antibodies decreased cell transmigration by about 50%. Combination of an MMP inhibitor with anti-CD87 antibodies had no additive effect. These data show that 5-oxo-ETE is an efficient promoter of eosinophil transmigration in vitro, and is much more potent in this respect than PAF. The data suggest that 5-oxo-ETE could play an important role in eosinophil recruitment in vivo. Moreover, they demonstrate that in addition to MMP, the plasmin/plasminogen system could be involved in eosinophil transmigration.

Adult↗
PubMed1995

Activation of the Fas receptor on lung eosinophils leads to apoptosis and the resolution of eosinophilic inflammation of the airways.

While considerable progress has been made in understanding the events by which eosinophils accumulate in various pathophysiological conditions, the mechanisms controlling the resolution of eosinophilic inflammation are poorly understood. In the present study, we demonstrate that lung eosinophils obtained by bronchoalveolar lavage (BAL) after aerosol allergen provocation of immunized mice expressed the Fas receptor. Stimulation of purified eosinophils in vitro with a monoclonal anti-Fas mAb (1 ng-1 microg/ml) induced a dose/time dependent loss of cell viability from 24-72 h. Measurement of DNA fragmentation with propidium iodide confirmed that anti-Fas induced eosinophil death by apoptosis. While incubation with IL-3, IL-5, or GM-CSF prevented spontaneous apoptosis, these factors failed to prevent anti-Fas induced apoptosis. Administration of anti-Fas mAb to the lungs after the induction of a lung eosinophilia increased the number of peroxidase positive macrophages in BAL fluid 4-12 h later which was followed by a marked reduction in the number of eosinophils in the airways. Importantly, Fas-mediated resolution of eosinophilic inflammation occurred in the absence of any overt secondary inflammatory changes in the lungs. We speculate that defects in this pathway may at least in part explain the chronic eosinophilic inflammation often observed in the lungs of asthmatic individuals.

Animals↗
PubMed1984

Circulating eosinophil colony-forming cells in pure eosinophil aplasia.

Using a methylcellulose clonal culture method, we found eosinophil colony-forming cells in the blood of two patients: a 46-year-old white woman with a long history of urticaria and allergic rhinitis and complete absence of eosinophils secondary to IgG-mediated and complement-mediated destruction of her eosinophils; and a white woman with a history of allergic rhinitis and asthma and a complete absence of eosinophils in her peripheral blood. Addition of the patients' plasma or IgG to cultures of peripheral blood mononuclear cells derived from normal persons or the patients inhibited formation of eosinophil colonies without influencing colony formation in other hemopoietic cell lineages. In contrast, normal plasma or IgG had no effect on the formation of eosinophil colonies. That the IgG-mediated cytotoxic activity of eosinophils prevents the expression of an apparently normal eosinophilopoietic potential suggests an autoimmune basis for the eosinophil aplasia.

Agranulocytosis↗