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Background: Eosinophilic cationic protein (ECP) is associated with airway inflammation and asthma. However, the clinical value of measuring ECP in childhood asthma is not fully known. We aimed to study the diagnostic performance of serum ECP and other common asthma biomarkers, individually and in combinations. Methods: In a cross-sectional study, 5–16-year-old children with current asthma (CA) (n = 37), transient asthma (TA) (n = 43), (previous history of wheezing/asthma), and healthy children (HC) (n = 86) were investigated for ECP, blood eosinophil count (B-Eos), fractional exhaled nitric oxide (FeNO), and lung function, i.e., spirometry (forced expiratory volume during the first second [FEV1]/forced vital capacity [FVC] ratio). Results: Both ECP and B-Eos were higher in CA compared to TA (p < 0.01) and HC (p < 0.0001). ECP and B-Eos were also higher in TA compared to HC (p < 0.05 and p < 0.001, respectively). FeNO was higher in CA (p < 0.0001) and TA (p < 0.01) compared to HC but similar between the asthma groups. The FEV1/FVC ratio was lower in CA compared to TA and HC (both p < 0.01) but similar between TA and HC. The best diagnostic performance regarding CA was found for ECP and B-Eos with receiver operating characteristics area under curve (AUC) of 0.801 and 0.810, respectively. The optimal cutoff for ECP (29 μg/L) yielded a sensitivity and specificity of 70.3% and 81.4%. The corresponding AUCs for FeNO and FEV1/FVC were 0.732 and 0.670, respectively. ECP and B-Eos showed the highest AUCs (0.669 and 0.673) for differentiation between CA and TA. Combining ECP with FeNO and FEV1/FVC increased the odds ratio (OR) for having CA from OR 3.97–10.3 for the single biomarkers to OR 20.2 (95% confidence interval: 5.76–68.6). Conclusion: Our results show that serum ECP is a reliable biomarker in the diagnosis of childhood asthma, with additional value in combination with FeNO and FEV1/FVC, and that ECP can be an alternative to B-Eos. [ABSTRACT FROM AUTHOR]

Background: It has been suggested that there is a complex interaction between microbiota and various human diseases. Some bacteria have been reported to be involved in the inception and progression of asthma, and others in the protection against asthma. We know very little about the mechanisms by which bacteria do harm or good with regard to asthma. This study investigated whether bacteria exert differential effects on the functions of eosinophils, major effector cells in airway inflammation in asthma. Methods: Eosinophils were purified from healthy adult volunteers by Percoll density gradient centrifugation and negative immunomagnetic bead selection using anti-CD16 microbeads. Three kinds of heat-killed bacteria that have been implicated in asthma, namely Staphylococcus aureus (SA), Haemophilus influenzae (HI) and a Prevotella sp. (PS), were tested for their effects on the secretion of eosinophil-derived neurotoxin (EDN), the generation of superoxides and the production of cytokines/chemokines. Results: SA, but not HI or PS, induced significant EDN release in a dose-dependent manner. Superoxide generation was significantly enhanced by each of the bacterial species, but most strongly by SA, which induced significantly greater TNF-α production by eosinophils than either HI or PS. Conversely, interleukin 10, an anti-inflammatory cytokine, was more strongly induced by HI and PS than by SA. Conclusions: Bacteria exert differential effects on eosinophils. Based on these results, SA may be involved in the exacerbation of, and HI and PS in the inhibition of, eosinophilic inflammation in asthma. Copyright © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: In developed countries, increasing food allergy prevalence and concern regarding food allergies have been reported. Although the use of complementary and alternative medicine (CAM) for the treatment of allergic diseases has increased in some Western countries, the actual proportion and patterns of CAM use for pediatric food allergies in Japan are still unknown. Methods: Fourteen allergy centers in Japan participated in the study using a questionnaire survey regarding the use of CAM by pediatric patients. A diagnosis of food allergy was made at each hospital by pediatric allergists. Results: Surveys were completed by parents/guardians, and data were collected for a total of 962 pediatric food-allergic patients. Overall, 8.4% of the participants used CAM to treat a food allergy. The major CAM therapies used were herbal teas (22.2%), including several Japanese herbal teas, Chinese herbal medicine (18.5%) and lactic acid bacteria (16%). Among the participants using CAM to treat food allergy, 13.6% thought that the CAM being used was very effective, while 11.1% of participants thought that CAM caused some type of side effect. Conclusions: Our study is the first large-scale national survey regarding the use of CAM in pediatric patients with food allergies in Japan. Unlike in the USA, which has a higher rate of CAM use (17%), approximately 8.4% of food-allergic patients used CAM in Japan. Interestingly, the major types of CAM used in Japan differed from those used in the USA. Cultural differences and food customs may affect the use of CAM. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Epidemiological studies suggest that vitamin D may be protective against the inception and exacerbation of allergic diseases. However, the direct effect of vitamin D on eosinophils, the major effector cells in allergic inflammation, is not known. It has been reported that C-X-C chemokine receptor type 4 (CXCR4) in eosinophils is induced in non-Th2 cytokine milieu or in response to glucocorticoids, recruiting the cell to noninflammatory sites. Objectives: To test whether 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3 or calcitriol], the active metabolite of vitamin D, acts directly on eosinophils to induce upregulation of CXCR4. Methods: Peripheral blood eosinophils from normal volunteers were isolated by CD16 immunomagnetic beads. Vitamin D receptor (VDR) expression was detected by RT-PCR. Eosinophils were cultured with 1,25-(OH)2D3 and the survival and expression of CXCR4 on eosinophils were measured by flowcytometry. Eosinophil migration by CXCL-12/SDF-1 in the presence of 1,25-(OH)2D3 was also analyzed. Results: Eosinophils expressed VDR. 1,25-(OH)2D3 prolonged eosinophil survival and upregulated eosinophil surface expression of CXCR4 in a concentration-dependent manner. Interleukin (IL)-5 significantly reduced CXCR4 expression and migration induced by the ligand CXCL-12/SDF-1. 1,25-(OH)2D3 reversed the negative effects of IL-5 on the CXCR4-CXCL12 pathway. Conclusion: 1,25-(OH)2D3 regulates CXCR4 expression in eosinophils. The mechanism may be involved in eosinophil recruitment to noninflammatory sites where the ligand of CXCR4 is constitutively expressed. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Kimura disease is a rare disorder of unknown etiology, characterized by the presence of benign subcutaneous granuloma, marked peripheral blood eosinophilia and elevation of the immunglobulin E (IgE) serum level. Here, we present a case of a 12-year-old boy with Kimura disease who had a history of repeated severe influenza virus A infection. Along with the characteristic histological findings of granuloma, including eosinophil infiltration, enzyme-linked immunospot assay showed elevated numbers of IL-5- and IL-10-producing cells in the peripheral blood. Immunohistochemical evaluation, however, did not detect IL-5 in the tissue. Possible cytokine dysregulation in Kimura disease was suggested, but the pathogenesis remains unclear. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Viral respiratory tract infections play an important role in the inception and exacerbation of asthma. Eosinophils, major effector cells in asthma, often accumulate in the airways during viral infections and are possibly activated by respiratory RNA viruses through Toll-like receptor (TLR) 7. We investigated the effect of a β2-agonist, i.e. procaterol, and a corticosteroid, i.e. budesonide, that are commonly used for viral-induced asthma, on TLR7 ligand-induced activation of eosinophils in vitro. Methods: Purified peripheral blood eosinophils were incubated with procaterol and/or budesonide and stimulated with a TLR7 ligand, i.e. R-837. Expression of CD11b was analyzed by flow cytometry. Superoxide generation was measured via the cytochrome C reduction method. IL-8 in the supernatants was assayed by ELISA. Results: Although procaterol or budesonide alone did not inhibit R-837-induced CD11b expression, combinations of the 2 drugs significantly inhibited CD11b. Likewise, the combinations significantly inhibited O2- generation at low concentrations. Budesonide significantly inhibited R-837-induced IL-8 production in a concentration-dependent manner, and procaterol potentiated inhibition by budesonide although single-agent procaterol had no effect. Conclusion: A combination of procaterol and budesonide inhibits the TLR7-mediated effector function of eosinophils, indicating their possible anti-inflammatory effect for virus-induced asthma. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Hypereosinophilic syndrome (HES) is a heterogeneous group of uncommon disorders characterized by the presence of marked peripheral blood eosinophilia and tissue eosinophilia, resulting in a wide variety of clinical manifestations. We present the case of an 8-year-old boy with HES. He complained of recurrent abdominal pain, general fatigue, and diarrhea. Laboratory data showed marked eosinophilia, elevated total IgE with positive specific IgE antibodies to common inhalant and food allergens, and elevated serum CCL17/TARC. A chest CT scan revealed central bronchiectasis, bronchial wall thickening, a mosaic attenuation pattern, and multiple small nodules in lung parenchyma; abdominal CT showed a thickened bladder wall. Gastrointestinal endoscopy revealed scarring in the gastric mucosa and mucosal erosion in the duodenum. Immunohistochemical examination demonstrated numerous eosinophil infiltrations with extensive extracellular eosinophil major basic protein deposition in the gastric mucosa. Only high-dose oral steroid was effective and cyclosporine appeared to have a steroid-sparing effect. HES is extraordinary rare in children and the long-term prognosis in pediatric HES is not well known. Comprehensive diagnostic procedures are vital for the early detection and management of complications in pediatric HES. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Few studies have investigated the complementary effects of long-term oral administration of Lactobacillus acidophilus on traditional medical therapy in the treatment of patients with atopic dermatitis (AD). Methods: The Atopic Dermatitis Area and Severity Index was used to evaluate AD severity. Symptom severity was assessed using the symptom score. The effect of medical therapy was evaluated by adding the medication score, calculated as the sum of each product of the amount of steroid ointment used for therapy and its designated strength graded on a 4-point scale, to the symptom score. The complementary effect of long-term oral administration of L. acidophilus strain L-92 (L-92) as a probiotic or biogenic strain in patients with AD was evaluated using the symptom-medication score, which was calculated as the sum of the symptom score and medication score. Both a preliminary casuistic study and a double-blinded, placebo-controlled study were performed to evaluate the effects of L-92 on the symptoms of AD in children. Results: Orally administered L-92 significantly ameliorated the symptoms of AD in Japanese children. L-92 also affected the serum concentrations of thymus and activation-regulated chemokine in a time-dependent manner.Conclusions: The results of the preliminary trial and the double-blinded, placebo-controlled study revealed a complementary effect of oral L-92 on the standard medical therapy (topical application of a steroid ointment) in patients with AD that was mediated, at least in part, by alterations in the Th1/Th2 balance. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Recent studies suggest that probiotics alleviate pathophysiological processes of allergic diseases and inflammatory bowel diseases, whereas ‘non-probiotic’ microflora has negative effects. However, the underlying mechanisms are not well known, especially in relation to eosinophils, the major effector cells of these inflammatory diseases. Objective: To investigate the effects of probiotic Bifidobacterium bifidum (BB) on human eosinophil functions compared with pathogenic Clostridium difficile (CD). Methods: Peripheral human eosinophils were cultured with heat-killed BB or CD. FISH-labeled CD and BB were incubated with eosinophils visualized by confocal laser scanning microscopy. Superoxide generation and degranulation of eosinophils were measured with the cytochrome c reduction method and the eosinophil-derived neurotoxin (EDN) release assay, respectively. Results: Confocal microscopy revealed that Cy3-labeled CD and BB were apparently ingested by eosinophils. Both bacteria induced minimal superoxide generation. However, CD elicited significantly higher EDN release than BB. GM-CSF significantly enhanced EDN release by CD but not by BB. Bacterial-induced EDN release was calcium dependent. Conclusion: The beneficial effect of probiotic BB might be explained, at least in part, by its ability to decrease EDN release from eosinophils compared with ‘pathogenic’ CD. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Japanese cedar pollen is by far the most important cause of allergic rhinitis in Japan. In this study, we assessed the induction of blocking antibody during specific immunotherapy (SIT) using a recently standardized allergen extract from Japanese cedar pollen. Methods: Basophils from nonallergic subjects were passively sensitized with serum samples prepared from pollinosis patients before and after SIT; all patients showed good clinical efficacy. The cells were then stimulated with the standardized allergen, and histamine release was measured. In most experiments, the basophil stimulation buffer contained 1% serum. Results: Pollinosis patients’ sera obtained both before and after SIT showed essentially similar sensitizing capacity for basophils. Basophil degranulation in response to a relatively low concentration of pollen extract was effectively suppressed by addition of post-SIT serum samples, indicating the presence of blocking antibody. The blocking antibody was IgG, and its potency varied widely among the donor patients. Conclusions: The standardized allergen extract from Japanese cedar pollen is useful not only for clinical application in SIT, but also for testing for induction of blocking antibody during SIT. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Recent evidence suggests that both neutrophilic and eosinophilic inflammation persist in the airways of patients with severe asthma. Mechanisms for interaction between neutrophils and eosinophils are still to be understood. Since eosinophils express protease-activated receptor 2, neutrophil-derived serine proteases may activate eosinophils. Objective: We investigated the effect of neutrophil serine proteases on eosinophil effector functions. Methods: Peripheral blood eosinophils were stimulated with elastase, cathepsin G and proteinase 3. Superoxide generation was quantitated with the cytochrome C reduction method. A panel of cytokines and chemokines in the culture supernatants were measured with a multiplex beads array system. Effects of an elastase inhibitor, sivelestat, and a serine protease inhibitor, PMSF, on the protease-induced reactions were also tested. Results: Neutrophil proteases significantly induced superoxide production from eosinophils. Elastase was the most potent among them. Sivelestat and PMSF inhibited the reaction. The proteases induced production of IL-6, IL-8, TNF-α and GRO-α, that have a possible connection with neutrophilic inflammation. Conclusion: Neutrophil proteases activate eosinophils to produce superoxide, proinflammatory cytokines and neutrophilotactic chemokines and may further aggravate airway inflammation in patients with severe asthma. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Rush immunotherapy (RIT) can confer rapid clinical benefit on patients with allergic rhinitis or asthma. However, biomarkers representing mechanisms for the efficacy of RIT are still to be established. CD203c is a basophil activation marker known to be upregulated by cross-linking of the FcεRIα receptor and may serve as a useful marker. Objective: We sought to investigate the changes in allergen-induced CD203c expression in patients with Japanese cedar pollen (JCP) pollinosis who received RIT. Methods: Nine patients treated with RIT were enrolled in the study. Whole blood was incubated with various concentrations of JCP extract. CD203c expression on basophils was quantitated by means of flow cytometry. JCP-specific IgG4 levels in sera were measured with ELISA. Basophil histamine release, CAP-RAST to JCP (JCP-IgE) and total IgE were also examined. The biomarkers listed above were evaluated before and sequentially after RIT. Symptom and quality of life scores were obtained during pre- and posttreatment pollen seasons. Results: All patients showed significant improvement in symptom and quality of life scores after RIT. Serum JCP-specific IgG4 titers were significantly elevated at 1 month and remained at high levels 12 months after the treatment. Stimulation with JCP extract induced enhancement of basophil CD203c expression in a concentration-dependent manner except for 2 subjects in whom no increase in CD203c by an anti-IgE antibody was observed (nonresponders). Significant reductions in the responses were observed in 4 subjects after RIT (reduction in CD203c expression, RCE) whereas no changes were seen in 3 subjects (non-RCE). RCE subjects were older than non-RCE counterparts, with mean ages of 20 and 12 years, respectively. No significant changes in JCP-specific IgE and total IgE levels were seen before and after RIT. Conclusion: Allergen-induced CD203c expression in basophils may represent, at least in part, the cellular mechanism for the therapeutic responses to RIT for JCP pollinosis. However, further larger-scale studies to confirm the utility of the test are necessary. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Eosinophils may play an important role in the pathogenesis of airway remodeling in asthma through the production of various fibrogenic cytokines such as transforming growth factor-β1 (TGF-β1). Cysteinyl leukotrienes are also suggested to be involved in remodeling with their potential to induce proliferation of airway smooth muscle cells. Since massive eosinophil infiltration and the release of cysteinyl leukotrienes in airway secretions are often seen in asthma, we hypothesized that cysteinyl leukotrienes may be involved in airway remodeling through induction of TGF-β1 from eosinophils. Peripheral blood eosinophils were cultured with leukotriene D4 (LTD4) and/or interleukin-5 (IL-5) or granulocyte colony-stimulating factor (GM-CSF) for 16 h and gene expression of TGF-β1 was quantified with real-time PCR. A combination of LTD4 and IL-5 or LTD4 and GM-CSF synergistically induced TGF-β1 expression in eosinophils although stimulation with single factor, LTD4, IL-5 or GM-CSF did not induce the gene expression. LTD4 also induced significant gene expression in eosinophils cultured in an intercellular adhesion molecule-1-coated plate. The results suggested that CysLTs stimulate eosinophils to induce TGF-β1 production in allergic inflammation where IL-5 and GM-CSF are abundant and may be involved in the pathogenesis of airway remodeling. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: The cysteinyl leukotrienes (CysLTs) mediate their biological actions through two receptors: CysLT[sub 1] receptor and CysLT[sub 2] receptor. Objective: This study was undertaken to examine the direct effects of CysLTs on eosinophils, such as chemotaxis and degranulation, focusing on CysLT[sub 1] . Methods: Eosinophils were isolated from venous blood from normal volunteers who had no history of allergy (purity >99%). They were subjected to reverse transcription-PCR analysis and flow-cytometric analysis for CysLT[sub 1] . Binding assays were performed with [[sup 3] H]LTD[sub 4] . Purified eosinophils loaded with Fura-2 acetoxymethyl ester were stimulated with CysLTs, and Ca[sup 2+] influx was measured. Eosinophil migration in response to CysLTs was measured using a 96-well multiwell Boyden chamber. Eosinophils were treated with LTD[sub 4] at 10[sup –6] M for 60 min followed by incubation for 4 h at 37°C in the presence or absence of IL-5 and eosinophil-derived neurotoxin (EDN) release was evaluated. Results: The expression of the mRNA and protein of CysLT[sub 1] on eosinophils and [[sup 3] H]LTD[sub 4] -specific binding to eosinophils were observed. Neither Th1 cytokine (IFN-γ) nor Th2 cytokines (IL-4 or IL-5) affected CysLT[sub 1] expression in eosinophils. CysLTs induced an increase in intracellular free Ca[sup 2+] in eosinophils via CysLT[sub 1] , as suggested by the efficient inhibition by a CysLT[sub 1] antagonist, pranlukast, in addition to the rank order of potency being LTD[sub 4] , LTC[sub 4] and LTE[sub 4] . LTD[sub 4] stimulated eosinophils to migrate at 10[sup –6] M via CysLT[sub 1] . LTE[sub 4] also induced significant eosinophil migration at 10[sup –6] M. LTD[sub 4] enhanced EDN release induced by IL-5 via CysLT[sub 1] . Conclusion: CysLTs induce migration and enhance degranulation in eosinophils via CysLT[sub 1] . Accordingly, interaction of CysLTs and CysLT[sub 1] on eosinophils has the potential to play a prominent role in the pathophysiology of asthma.Copyright © 2002 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Signals via chemokine receptors play an important role in the accumulation of eosinophils at allergic inflammatory sites. Eosinophils constitutively express CC chemokine receptor 3 (CCR3) and, to a lesser extent, CCR1. CCR3 is mainly responsible for migration of resting eosinophils, and its specific ligand, eotaxin, represents the most potent chemoattractant for eosinophils. Some reports also suggest the expression of CXC chemokine receptor 1 (CXCR1) and/or CXCR2 in eosinophils. In addition, we recently reported the functional expression of CXCR4. The ligand of CXCR4, stromal cell-derived factor-1 (SDF-1), was able to induce a strong migratory response comparable to that by eotaxin. In contrast to the CCR3/eotaxin system which is mainly regulated at the level of ligand production, the CXCR4/SDF-1 system is regulated at the level of receptor expression. CXCR4 expression was completely attenuated by IL-4 and IL-5 and upregulated by IFN-γ and dexamethasone, while CCR3 expression was only marginally affected. The balance between the biological effects of these chemokine systems may affect the distribution and migration of eosinophils.Copyright © 2001 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Recent studies have demonstrated that eosinophils from allergic patients express low levels of FcεRI on their surface, but the regulatory mechanisms of eosinophil surface FcεRI expression are not fully understood. We investigated whether IL-4 and IgE, which are reported to regulate surface FcεRI expression on human mast cells, are able to affect surface FcεRI expression in normal human eosinophils. Methods: Eosinophils purified from peripheral blood were cultured with IL-5 and with or without IL-4 and/or IgE, and surface FcεRI expression was analyzed by flow cytometry using an anti-FcεRI mAb, CRA-1. Results: Apparent FcεRI expression (∼1% of mast cell FcεRI levels) was observed in eosinophils cultured with both IL-4 and IgE. A combination of IL-4 (≥1 ng/ml) and IgE (≥ 0.5 μg/ml) was necessary for the maximal induction of surface FcεRI expression. In the presence of IL-4 and IgE, eosinophils cultured for 2 days demonstrated low but statistically significant levels of surface FcεRI, which reached a plateau after 7 days of culture. However, cross-linkage of surface FcεRI molecules by CRA-1 or anti-IgE did not induce any eosinophil activation. Conclusions: IL-4 and IgE can affect the levels of surface FcεRI on normal human eosinophils. FcεRI expression on eosinophils may be regulated by a mechanism similar to that in mast cells.Copyright © 2001 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Measurement of eosinophil cationic protein (ECP) in serum has been utilized as a marker for allergic inflammation. The serum level of ECP represents the level found in vivo plus additional proteins released in vitro from peripheral blood eosinophils during the coagulation period. The mechanisms of release, however, are unclear. We investigated a possible involvement of adhesion molecules in the ECP release. Materials and Methods: Venous blood was drawn in the presence of EDTA from allergic donors. The blood was incubated with neutralizing monoclonal antibodies to CD18, CD11a, CD11b, CD29, CD49d, CD54, α[sub 4] β[sub 7] , or isotype-matched control antibodies, respectively, at 4°C for 30 min. Calcium gluconate (calcium) was then added to induce coagulation. The blood was further incubated for 90 min and centrifuged to obtain the serum. ECP in the serum was measured with RIA. In some experiments, purified eosinophils were incubated with plasma and calcium, then ECP in the supernatants was assayed. Results: ECP in the samples with calcium was significantly higher than in those without calcium. Purified eosinophils released ECP upon plasma coagulation. Anti-CD18, CD49d, and α[sub 4] β[sub 7] antibodies significantly suppressed ECP levels in the serum. Conclusions: These results suggest that ECP release in the serum is calcium and plasma coagulation-dependent and that cell adhesion through α[sub L] β[sub 2] , α[sub M] β[sub 2] , α[sub 4] β[sub 1] and α[sub 4] β[sub 7] integrins is at least in part responsible for ECP release. [ABSTRACT FROM AUTHOR]

Background: Matrix metalloproteinases (MMPs) are major contributors to tumor invasion, remodeling of connective tissue and infiltration of inflammatory cells and may be important mediators in developing allergic inflammation. Overexpression of MMP-9 mRNA by eosinophils in the asthmatic airways has been reported. To clarify the relative significance of MMP as an inflammatory mediator from eosinophils, we determined the content of MMP-9 in the peripheral blood eosinophils and compared it with the other leukocyte fractions. Methods: Peripheral blood eosinophils, neutrophils, and mononuclear cells were purified from normal and allergic donors with Percoll gradient centrifugation and CD16 negative selection. Cell lysate and culture supernatants stimulated with IL-5, PAF, and PMA were tested for MMP-9 with gelatin zymography and ELISA. Results: The amount of MMP-9 in highly purified eosinophils, neutrophils, and mononuclear cells was 2.5 ± 0.9, 4,073 ± 581, and 7.6 ± 1.4 ng/5 × 10[sup 6] cells, respectively. There was no difference in MMP-9 content of eosinophils between normal donors and patients with asthma. Culture of peripheral blood eosinophils with IL-5 for 4 days did not induce MMP-9 production. The stimulation of eosinophils with PMA and other secretogogues caused only small amounts of MMP-9 secretion as compared with neutrophils. Conclusions: These findings suggest that circulating eosinophils normally have only small amounts of MMP-9 and that eosinophils may need complex activation signals to produce significant amounts of MMP as seen in tissues of allergic inflammation. [ABSTRACT FROM AUTHOR]

Presents an overview of several studies on allergic inflammation. Role of eosinophils in the pathogenesis of asthma; Reduction of eosinophil in the lung and peripheral blood by a humanized anti-interleukin-5 monoclonal antibody (SB-240563); Topics presented and discussed at the 14th Annual Workshop on Eosinophils in Allergy and Related Diseases 2001.

A preface for the May 2008 issue of the "International Archives of Allergy and Immunology" is presented.

Presents the table of contents of the May 2, 2002 issue of the "International Archives of Allergy and Immunology."