The eosinophil, eosinophilia, and eosinophil-related disorders. IV. Eosinophil related disorders (continued).
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Eosinophilia↗
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Eosinophilic granuloma, eosinophilic gastroenteritis and eosinophilic peritonitis.
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Adrenal Cortex Hormones↗
Eosinophilic infiltration of the esophagus: gastroesophageal reflux versus eosinophilic esophagitis in children--discussion on daily practice.
BACKGROUND/PURPOSE: Children presenting with persistent symptoms attributed to gastroesophaeal reflux disease (GERD) that are unresponsive to both medical and surgical therapies are commonly submitted to esophageal biopsies, the results of which show an abnormal presence of eosinophils. In this setting, eosinophilic esophagitis may be the correct diagnosis. The purpose of this report is to clarify the importance of esophageal eosinophilic infiltration, regardless of whether associated with acid reflux, ie, as an independent symptomatic entity, when treating a patient with refractory GERD. METHODS: Two boys, aged 8 and 7 years, had the classic symptoms of GERD. They were treated with antacid without improvement of the esophagic lesions. Subsequent esophageal biopsy results showed marked eosinophilic infiltration. From this moment on, eosinophilic esophagitis started to be considered the main diagnosis. RESULTS: Although eosinophilic infiltration caused by GERD is very frequently found in esophageal biopsy, in case of refractory drug treatment and microscopic findings of a great number of eosinophils and mast cells, eosinophilic esophagitis must be considered. This disease is better treated with corticoids instead of antacid drugs. It explains the reason some patients do not respond to antacid and surgical treatment and remain symptomatic with esophagic lesions. CONCLUSIONS: In refractory cases of GERD, eosinophilic esophagitis must be considered before any surgical measure.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Mechanisms of acute eosinophilic inflammation in a case of acute eosinophilic pneumonia in a 14-year-old girl.
BACKGROUND: Acute eosinophilic pneumonia (AEP) is characterized by respiratory distress, eosinophilic infiltration in the lung, acute onset, resolution of symptoms with corticosteroids and the absence of relapse. Studies to identify the pathophysiology of AEP in adults have demonstrated eosinophil activation in the BAL fluid, and the presence of high levels of interleukin 5 (IL-5) in the BAL. OBJECTIVE: To investigate the pathophysiology of AEP with pleural effusion in a paediatric patient. METHODS: ECP levels in the BALand pleural fluid was determined by radioimmunoassay. IL-5 and GM-CSF concentrations in the BAL and pleural fluid were measured by Elisa. Immunohistochemistry studies performed on open lung biopsy included a specific ICAM-1 immunostaining and a ECP specific immunostaining (EG2+). RESULTS: High levels of ECP were found in the BAL (5 microg/L) and pleural fluid (750 microg/L) demonstrating eosinophil activation at these sites. Immunohistochemistry illustrated activated (EG2+) eosinophils in the interalveolar septa and alveolar space and detected increased expression of ICAM-1 on alveolar epithelial cells. High levels of IL-5 were measured in the BAL (1334 pg/mL) and pleural fluid (7014 pg/mL), while elevated concentrations of GM-CSF (150 pg/mL) were found in the BAL. CONCLUSION: We conclude that in this paediatric patient with AEP activated eosinophils were present in the BAL fluid, in the interalveolar septa and in the pleural space while increased ICAM-1 expression was detected on alveolar epithelial cells, contributing, at least partly, for their adhesive interactions. IL-5 and GM-CSF are likely important to the massive eosinophil recruitment and activation in the lung, while IL-5 is probably related to eosinophil accumulation and activation in the pleural space. Thus, lung generation of eosinophil-active cytokines is central to the pathophysiology of AEP in paediatric patients.
Acute Disease↗
Ovalbumin challenge following immunization elicits recruitment of eosinophils but not bronchial hyperresponsiveness in guinea-pigs: time course and relationship to eosinophil activation status.
Eosinophils are known to be present in the airways of allergic asthmatics, and have been suggested to contribute to the pathophysiological changes accompanying this condition, particularly hyperresponsiveness to airway spasmogens. However, a causal relationship between pulmonary eosinophil accumulation and bronchial hyperresponsiveness in asthma is not proven. In the present study, the time course of pulmonary cell influx was investigated in an immunized guinea-pig model. Eosinophil activation status was also determined together with the bronchial responsiveness to histamine. Guinea-pigs were sensitized [20 micrograms ovalbumin (OVA) per animal in A1(OH)3 (0.5 ml) i.p.] and subsequently challenged with aerosolized OVA (100 micrograms/ml) for 1 h 18-21 days later. At different time points (1 h to 72 h) after OVA challenge, bronchial responses to i.v. histamine were measured and bronchoalveolar lavage (BAL) was performed to assess pulmonary cell influx. Eosinophil peroxidase (EPO) and total protein levels were measured in BAL fluid supernatants. Exposure of sensitized animals to aerosolized OVA produced a significant increase (P < 0.05 vs. sham immunized) in eosinophil infiltration 24 h later which was sustained up to 72 h. Despite this, OVA challenge did not cause either eosinophil activation, as measured by EPO release, or bronchial hyperresponsiveness to histamine at any of the time points examined. These data show that allergen challenge of sensitized guinea-pigs can elicit airway eosinophil accumulation without accompanying airways hyperresponsiveness or eosinophil activation.
Animals↗
Mechanism of nitrite oxidation by eosinophil peroxidase: implications for oxidant production and nitration by eosinophils.
Eosinophil peroxidase is a haem enzyme of eosinophils that is implicated in oxidative tissue injury in asthma. It uses hydrogen peroxide to oxidize thiocyanate and bromide to their respective hypohalous acids. Nitrite is also a substrate for eosinophil peroxidase. We have investigated the mechanisms by which the enzyme oxidizes nitrite. Nitrite was very effective at inhibiting hypothiocyanous acid ('cyanosulphenic acid') and hypobromous acid production. Spectral studies showed that nitrite reduced the enzyme to its compound II form, which is a redox intermediate containing Fe(IV) in the haem active site. Compound II does not oxidize thiocyanate or bromide. These results demonstrate that nitrite is readily oxidized by compound I, which contains Fe(V) at the active site. However, it reacts more slowly with compound II. The observed rate constant for reduction of compound II by nitrite was determined to be 5.6x10(3) M(-1) x s(-1). Eosinophils were at least 4-fold more effective at promoting nitration of a heptapeptide than neutrophils. This result is explained by our finding that nitrite reacts 10-fold faster with compound II of eosinophil peroxidase than with the analogous redox intermediate of myeloperoxidase. Nitration by eosinophils was increased 3-fold by superoxide dismutase, which indicates that superoxide interferes with nitration. We propose that at sites of eosinophilic inflammation, low concentrations of nitrite will retard oxidant production by eosinophil peroxidase, whereas at higher concentrations nitrogen dioxide will be a major oxidant formed by these cells. The efficiency of protein nitration will be decreased by the diffusion-controlled reaction of superoxide with nitrogen dioxide.
Eosinophil Peroxidase↗
Topical steroid treatment of allergic rhinitis decreases nasal fluid TH2 cytokines, eosinophils, eosinophil cationic protein, and IgE but has no significant effect on IFN-gamma, IL-1beta, TNF-alpha, or neutrophils.
BACKGROUND: Topical treatment with glucocorticoids (GCs) is known to decrease eosinophils but not neutrophils in patients with allergic rhinitis. OBJECTIVE: We sought to examine whether the differential effects of GC treatment on eosinophils and neutrophils are mirrored by differential effects on T(H)1/T(H)2 cytokines and the neutrophil-associated cytokines IL-1beta and TNF-alpha. METHODS: Differential counts of eosinophils and neutrophils in nasal fluids from 60 children with seasonal allergic rhinitis treated with a topical GC were examined after staining with May-Grünwald-Giemsa stain. Nasal fluid levels of IFN-gamma, IL-4, IL-6, IL-10, IL-1beta, and TNF-alpha were examined with ELISA, and IgE and eosinophil cationic protein (ECP) levels were examined with RIA. RESULTS: After GC treatment, there was a statistically significant decrease of the T(H)2 cytokines IL-4, IL-6, and IL-10, as well as ECP and IgE. By contrast, there were no significant changes of the levels of IFN-gamma, IL-1beta, TNF-alpha, or neutrophils. In the GC-treated patients IL-1beta and TNF-alpha levels correlated with neutrophils and ECP, and IL-1beta correlated with eosinophils. Furthermore, ECP correlated with both eosinophils and neutrophils. Neither IL-1beta nor TNF-alpha correlated with IgE. Patients with high neutrophil counts after GC treatment were found to have significantly higher eosinophil counts and ECP than patients with low counts. CONCLUSIONS: The beneficial effects of topical treatment with GC in patients with allergic rhinitis could be attributed to downregulation of T(H)2 cytokines, with an ensuing decrease of eosinophils, ECP, and IgE. It is possible that neutrophils could counteract the beneficial effects of GCs by releasing the proinflammatory cytokines IL-1beta and TNF-alpha.
Administration, Topical↗
The synthetic PPARgamma agonist troglitazone inhibits IL-5-induced CD69 upregulation and eosinophil-derived neurotoxin release from eosinophils.
Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a nuclear receptor that regulates lipid metabolism. Recently, PPARgamma was reported to be a negative regulator in the immune system. Eosinophils also express PPARgamma, however, the role of PPARgamma in eosinophil functions is not well understood. Surface expression of CD69 and eosinophil-derived neurotoxin (EDN) release are well-known activation markers of eosinophils. We investigated the effect of a PPARgamma agonist on human eosinophil functions such as IL-5-induced CD69 surface expression and EDN release. IL-5 significantly induced eosinophil CD69 surface expression analyzed using flow cytometry and EDN release measured by ELISA. IL-5-induced eosinophil CD69 surface expression and EDN release were significantly inhibited by the synthetic PPARgamma agonist troglitazone, and these effects were reversed by a PPARgamma antagonist. The PPARgamma agonist troglitazone has a potent inhibitory effect on activation and degranulation of eosinophils, and it may be a therapeutic modality for the treatment of allergic diseases.
Analysis of Variance↗
Interleukin-12 inhibits eosinophil degranulation and migration but does not promote eosinophil apoptosis.
BACKGROUND: Animal and human studies demonstrated that interleukin (IL)-12, a Th1 cytokine, reduces blood and bronchial eosinophilia, and airway hyperreactivity. According to current concepts, these effects are mediated through the release of cytokines promoting eosinophil recruitment and activation. However, the presence of IL-12 receptors on eosinophils suggests that IL-12 also acts directly on eosinophils. We postulated that IL-12 directly modulates eosinophil functions and has the capacity to regulate eosinophil degranulation, migration and survival, in vitro. METHOD: Effects of IL- 12 on purified human blood eosinophils were evaluated for peroxidase (EPO) release, eotaxin-induced migration through a model of basement membrane (Matrigel), and survival. RESULTS: IL-12 inhibited 50% of PAF and secretory IgA-induced EPO release (n = 8, p < 0.001). IL-12 also reduced eotaxin-induced migration through Matrigel by 54 +/-6% (n = 6, p < 0.01). These effects were not explained by an IL-12-induced impaired viability or apoptosis. CONCLUSION: Our results demonstrate that IL-12 directly modulates eosinophil functions without promoting apoptosis and explain, at least in part, the effects of IL-12 on eosinophils observed in in vivo studies.
Apoptosis↗
The eosinophil component of the alveolitis in idiopathic pulmonary fibrosis. Signs of eosinophil activation in the lung are related to impaired lung function.
The number of eosinophils and the concentrations of eosinophil cationic protein (ECP), a specific granule constituent of eosinophil granulocytes, were measured in bronchoalveolar lavage (BAL) fluid from patients (n = 22) with idiopathic pulmonary fibrosis (IPF). The median recovery of eosinophils during lavage performance was 4% (range, zero to 49) of the nonepithelial cells and significantly increased compared with the recovery in healthy control subjects (less than 1%) and in control patients with sarcoidosis (1%; range, zero to 7). The median BAL fluid concentration of ECP was in IPF 13.3 micrograms/L (range, 2 to 118) and significantly increased compared with the concentrations in healthy control subjects (2.7 micrograms/L; range, less than 2 to 8) and in control patients (6.6 micrograms/L; range, less than 2 to 64). The BAL fluid concentrations of myeloperoxidase (MPO) were also significantly increased in IPF, indicating a local neutrophil activation. A significant correlation was found between BAL fluid ECP and MPO, suggesting a common activator of eosinophils and neutrophils. BAL fluid eosinophils and ECP correlated with the reduced diffusion capacity of the lung but not with vital capacity or forced expiratory volume. It is concluded that eosinophil activation is part of the inflammatory process in IPF. ECP and other cytotoxic eosinophil products may play a pathophysiologic role for the lung damage in this disease.
Adult↗
Cloning of the human eosinophil chemoattractant, eotaxin. Expression, receptor binding, and functional properties suggest a mechanism for the selective recruitment of eosinophils.
The CC chemokine eotaxin, identified in guinea pigs and also recently in mice, may be a key element for the selective recruitment of eosinophils to certain inflamed tissues. Using a partial mouse eotaxin CDNA probe, the human eotaxin gene was cloned and found to be 61.8 and 63.2% identical at the amino acid level to guinea pig and mouse eotaxin. Human eotaxin protein was a strong and specific eosinophil chemoattractant in vitro and was an effective eosinophil chemoattractant when injected into the skin of a rhesus monkey. Radiolabeled eotaxin was used to identify a high affinity receptor on eosinophils (0.52 nM Kd), expressed at 4.8 x 10(4) sites per cell. This receptor also bound RANTES and monocyte chemotactic protein-3 with lower affinity, but not macrophage inflammatory protein-1 alpha. Eotaxin could desensitize calcium responses of eosinophils to RANTES and monocyte chemotactic protein-3, although RANTES was able to only partially desensitize eosinophil calcium responses to eotaxin. Immunohistochemistry on human nasal polyp with antieotaxin mAbs showed that certain leukocytes as well as respiratory epithelium were intensely immunoreactive, and eosinophil infiltration occurred at sites of eotaxin upregulation. Thus eotaxin in humans is a potent and selective eosinophil chemoattractant that is expressed by a variety cell types in certain inflammatory conditions.
Amino Acid Sequence↗
Induction of hypodense eosinophils and nuclear hypersegmentation of eosinophils by various chemotactic factors and lymphokines in vitro.
We have previously reported pulmonary eosinophils in eosinophilic pneumonia (PIE syndrome) showed two characteristics: hypodensity and nuclear hypersegmentation. Our present working hypothesis is that the eosinophil chemotactic factor and certain lymphokines may be involved in the induction of these characteristic features. Therefore, we examined whether these stimuli can induce two characteristics in vitro. Results were as follows. 1) Chemoattracts (ECF-A, histamine and PAF) can induce both nuclear hypersegmentation and hypodense eosinophils. 2) Hypodense eosinophils can be induced earlier than induction of hypersegmented nuclei (hypodense eosinophils within three hours, hypersegmented nuclei: 12 hrs). 3) Furthermore, lymphokines can not induce hypodense eosinophil. 4) However, PHA-lymphocyte culture medium (PHALCM), gamma-IFN and IL-3 + GM-CSF can induce hypersegmented nuclei but IL-2 has no effect on nuclear segmentation of eosinophils.
Biological Factors↗
[Eosinophilic leukemia with cyclic eosinophilic leukocytosis].
A 36-year-old male was admitted to the Ehime University Hospital with anemia, eosinophilia and hepatosplenomegaly. Peripheral blood examination demonstrated severe anemia (Hb 7.1g/dl), thrombocytopenia (Plt 6.8 x 10(4)/microliters) and increase of peripheral leukocyte counts (53,000/microliters) with 32.0% of eosinophils which had lobulated nuclei, abnormal distribution of eosinophilic granules and a few vacuoles. The level of serum IgE was low (< 5IU/ml), while that of serum vitamin B12 was elevated. A diagnosis of eosinophilic leukemia was made. He was noted to have spontaneous fluctuations in his eosinophil and total leukocyte counts. To analyze the mechanism of cyclic eosinophilic leukocytosis, we examined eosinophil colony stimulating activity of the serum and plasma of the patient. These examination showed that eosinophil colony-stimulating activity was not found in his serum and plasma, and cyclic eosinophilic leukocytosis was due to the hemopoietic stem cell disorder.
Adult↗
Quantification of eosinophil cationic protein and eosinophils in nasal secretions of allergen-induced nasal inflammation.
By using the microsuction technique, a quantitative determination of eosinophil cationic protein (ECP) in nasal secretions was performed in 18 atopic patients and 10 healthy volunteers. The percentage of the eosinophils was counted by simple microscopic examination. In the control group, results showed that the percentage of the eosinophils was almost 0 (range: 0-0.7%), and the median baseline ECP concentration was measured at 105 ng/g (range: 2-281 ng/g). No significant changes in either eosinophils or ECP were observed in this group. In the patient group, there existed a significantly higher baseline percentage of eosinophils (median: 2.7%, range: 0-45%) than in the control group but not for baseline ECP concentration (median: 160 ng/g, range: 6-1475 ng/g). One hour after nasal allergen challenge (NAC), a significant (P < 0.01) increase was seen in the percentage of eosinophils of the nasal secretions and this was remained for 10 hours (median: 5.5-13.3%). However, the difference that occurred was that ECP reached its highest concentration (median: 401 ng/g, range: 32-2298 ng/g) only 24 hours after NAC, while the percentage of the eosinophils decreased. Our findings again support a role of migration and activation of eosinophils in the pathogenesis of nasal allergic reaction, especially during the late phase.
Adolescent↗
[The role of eosinophilic granulocytes for the pathogenesis of atopic dermatitis /neurodermatitis. Eosinophilic products as markers of disease activity].
Recent data provide increasing evidence for an immunological basis of atopic dermatitis (AD). Atopyspecific helper T cells (Th2-like T cells) may play a pathogenic role by producing and releasing cytokines that are relevant for the allergic inflammation, such as IL-4, IL-5 and other growth factors. It is suggested that eosinophils play a major role as effector cells mediating the pathogenetically important late-phase reaction, which is associated with significant destruction of the surrounding tissue. Accordingly, a significant preactivation of peripheral blood eosinophils was detected in AD patients, leading to enhanced susceptibility of these cells to distinct stimuli, such as IL-5. Toxic proteins, such as eosinophil cationic protein (ECP), which are 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 exerting their direct immunomodulatory effects. A pathogenic role of eosinophils in AD is further supported by the detection of these proteins in eczematous skin of the patients. Furthermore, recent data indicate 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 both in the clinical score and in serum ECP levels. These data clearly indicate that activated eosinophils are involved in the allergic inflammatory process in AD. Therefore, modulation of eosinophil activation could be an important pharmacologic modality for the treatment of AD in the future.
Allergens↗
[Chronic eosinophilic pneumonia involving eosinophil cationic protein and bone marrow cells].
A 64-year-old women presented with a dry cough. The common cold was diagnosed and she was given medication, but the symptom did not resolve. She came to our hospital, and multiple patchy shadows were seen on a chest X-ray film. Bronchoalveolar lavage fluid contained an abnormally high percentage of eosinophils. Microscopic examination of transbronchial lung biopsy specimens showed infiltration of eosinophils into the alveoli and alveolar septa. Chronic eosinophilic pneumonia was diagnosed. Analysis of bone marrow cells showed high percentages of mature eosinophilic cells, and blood serum had a high concentration of eosinophil cationic protein. An inhalation challenge test with methacholine revealed bronchial hypersensitivity and hyperresponsiveness. Prednisolone (30 mg/day) was given and the symptoms resolved. After steroid treatment, the patient was asymptomatic, although airway hyperresponsiveness remained. The concentration of eosinophil cationic protein in serum and the results of the methacholine inhalation test reflected the degree of chronic eosinophilic pneumonia, and the production of eosinophils in bone marrow was suppressed by steroid medication.
Blood Proteins↗
Chronic eosinophilic leukemia presenting with autoimmune hemolytic anemia and erythrophagocytosis by eosinophils.
Eosinophils function primarily as secretory cells and phagocytosis by eosinophils is rarely seen. We describe a case of chronic eosinophilic leukemia (CEL) in a 72-year-old male with a history of previously treated non-Hodgkin's lymphoma (NHL) presenting with erythrophagocytosis by eosinophils and an associated autoimmune hemolytic anemia (AIHA). This patient did not show evidence of relapsed NHL. The patient's blood showed a markedly elevated eosinophil count of 16 x 10(9)/L [normal 0-0.45 x 10(9)/L] on a background of myelodysplasia and features of AIHA. Prominent erythrophagocytosis by eosinophils was visualized in the blood and in the bone marrow. Numerous Charcot-Leyden crystals were also seen in the bone marrow amid increased numbers of eosinophils and the presence of dysplastic granulopoiesis. AIHA is rarely described in the setting of CEL. More significantly, this represents the first case report to describe erythrophagocytosis by eosinophils.
Aged↗
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↗