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PubMed1987

Eosinophilia in chimeric mice infected with Toxocara canis.

A marked strain variation in eosinophilia following oral infection with Toxocara canis eggs was observed in mice. Mutual radiation chimeras between high and low responder mice in terms of eosinophilia were made and compared with the respective donor and recipient for eosinophilia after the infection. As a result, the degree and time course of eosinophilia in chimeric mice were similar to those in donors. The result suggested that genes which regulate inheritance of the trait, marked eosinophilia in T. canis-infected mice, might be expressed in bone marrow derived cells.

Animals↗

PubMed1996

Fludarabine, as well as 2-chlorodeoxyadenosine, can induce eosinophilia during treatment of lymphoid malignancies.

We treated 25 patients suffering from low-grade lymphoid malignancies with nucleoside analogues. In 11 patients undergoing treatment with fludarabine, two patients with follicular lymphoma developed a marked absolute peripheral blood eosinophilia devoid of clinical symptoms which resolved without medical intervention. Of 15 patients treated with 2-chlorodeoxyadenosine, one patient with B-cell chronic lymphocytic leukaemia (CLL) experienced repeated episodes of eosinophilia that required steroid treatment. Eosinophilia in these three patients was not coupled to tumour lysis, and we found no correlation between the occurrence of eosinophilia and clinical response to treatment. Thus, for the first time, we can report eosinophilia as a side-effect of fludarabine treatment, and these are also the first published cases of this complication occurring in patients treated with nucleoside analogues for follicular lymphoma and CLL.

Aged↗

PubMedDate not supplied

Absence of late airway response despite increased airway responsiveness and eosinophilia in a murine model of asthma.

In asthmatics an immediate asthmatic response occurs after antigen provocation. Furthermore, asthmatic patients display airway hyperresponsiveness, accompanied by airway eosinophilia. In some patients late asthmatic responses can be detected. Many controversies still exist about the relations between the different airway responses and inflammatory cell infiltration, we therefore used a murine model to investigate associations between these phenomena. In this study we show the presence of antigen-induced early bronchoconstrictive responses, accompanied by increased serum mucosal mast cell protease-1 (MMCP-1) levels. However, we were unable to demonstrate late bronchoconstrictive responses either at the time when eosinophils start to infiltrate the lungs or when both airway hyperresponsiveness and eosinophilia are established. With sequential exposures to antigen, an association exists between development of airway hyperresponsiveness and eosinophilia. In contrast, resolution of this hyperreactivity appears to be dissociated from eosinophilia after stopping the antigen challenges. Based on these data, we conclude that mast cell degranulation is a plausible cause of early bronchoconstrictive responses. Furthermore, late bronchoconstrictive responses are not related to the infiltration of eosinophils or development of airway hyperresponsiveness in this murine model. Finally, we conclude that airway hyperresponsiveness and eosinophilia are only associated with each other during the induction phase and not after the final antigen challenge.

Animals↗

PubMed1970

Mechanism of eosinophilia. I. Factors affecting the eosinophil response of rats to Trichinella spiralis.

The phenomenon of eosinophilia was studied in rats using inoculation with Trichinella larvae as the experimental stimulus. Comparisons were made between the eosinophil response accompanying active infestation via the gastrointestinal tract and that resulting from parenteral inoculation of larvae or their products. A vigorous eosinophilia could be provoked by a single intravenous injection of intact parasites. In this circumstance the larvae lodged in the lungs causing an acute inflammatory reaction which led to their disintegration within 24 hr. Intraaortic injection also produced a significant response, whereas inoculation of the same number of parasites by the intramuscular, intraperitoneal, or subcutaneous routes did not cause eosinophilia. Eosinophilia likewise failed to develop if parasites were homogenized before intravenous injection, so that they were not arrested in the lungs. Antibody levels, as measured by a hemagglutination technique, using whole larval extract as antigen, did not correlate closely with the eosinophil response. The findings are interpreted as suggesting that increased eosinophil production is induced under some circumstances as a consequence of interaction between intact parasites and certain host cells in blood and tissue. No evidence was found for the existence of a specific constituent of the parasite capable of stimulating eosinophil production. Attention is directed to features of eosinophilia which fit with the concept that this phenomenon belongs in the category of immunologic reactions.

Animals↗

PubMed1998

Infection of mice with Mycobacterium bovis-Bacillus Calmette-Guérin (BCG) suppresses allergen-induced airway eosinophilia.

It has been proposed that the increase in prevalence and severity of atopic disorders inversely correlates with exposure to infectious diseases such as tuberculosis. We have investigated this issue by combining an intranasal Mycobacterium bovis-Bacillus Calmette-Guérin (BCG) infection with a murine model of allergen, (ovalbumin [OVA]) induced airway eosinophilia. BCG infection either 4 or 12 wk before allergen airway challenge resulted in a 90-95 and 60-70% reduction in eosinophilia within the lungs, respectively, compared to uninfected controls. The inhibition of airway eosinophilia correlated with a reduced level of IL-5 production by T cells from the lymph node draining the site of OVA challenge. Interestingly, BCG infection of the lung had no effect on IgG1 and IgE OVA-specific serum immunoglobulin or blood eosinophil levels. Furthermore, BCG-induced inhibition of airway eosinophilia was strongly reduced in interferon (IFN)-gamma receptor-deficient mice and could be partially reversed by intranasal IL-5 application. Intranasal BCG infections could also reduce the degree of lung eosinophilia and IL-5 produced by T cells after Nippostrongylus brasiliensis infection. Taken together, our data suggest that IFN-gamma produced during the T helper cell (Th)1 immune response against BCG suppresses the development of local inflammatory Th2 responses in the lung. Most importantly, this inhibition did not extend to the systemic immunoglobulin response against OVA. Our data support the view that mycobacterial infections have the potential to suppress the development of atopic disorders in humans.

Adjuvants, Immunologic↗

PubMed1998

Atypical pulmonary eosinophilia is mediated by a specific amino acid sequence of the attachment (G) protein of respiratory syncytial virus.

We analyzed the immune responses evoked by a series of overlapping peptides to better understand the molecular basis for respiratory syncytial virus (RSV) G protein-induced eosinophilia in BALB/c mice. In vitro stimulation of spleen cells from natural G protein-primed mice showed dominant proliferative and cytokine (interferon [IFN]-gamma and interleukin [IL]-5) responses to a peptide encompassing amino acids 184-198. Mice vaccinated with peptide 184- 198 conjugated to keyhole limpet hemocyanin showed significant pulmonary eosinophilia (39.5%) after challenge with live RSV. In contrast, mice immunized with a peptide (208-222) conjugate associated with induction of IFN-gamma secreting spleen cells did not exhibit pulmonary eosinophilia after challenge. The in vivo depletion of CD4(+) cells abrogated pulmonary eosinophilia in mice vaccinated with the peptide 184-198 conjugate, whereas the depletion of CD8(+) cells had a negligible effect. Therefore, we have identified an association between peptide 184- 198 of natural G protein and the CD4(+) T cell-mediated induction of pulmonary eosinophilia after live RSV challenge. Out of 43 human donors, 6 provided peripheral blood mononuclear cells that showed reactivity to G protein from RSV A2, 3 of which responded to peptide 184- 198. The results have important implications for the development of a vaccine against RSV.

Amino Acid Sequence↗

PubMed1997

Eosinophilia triggered by beta-interferon therapy for chronic hepatitis C.

The authors describe a case of eosinophilia occurring in an atopic patient suffering from chronic active hepatitis C following a 2-week course with beta-interferon. Since the most common causes of eosinophilia were ruled out by laboratory and instrumental investigations, the authors suggest a possible role of beta-interferon in triggering eosinophilia, in light of current beliefs about the factors modulating eosinophil growth, differentiation and survival. In particular, it has been supposed that the inhibitory effect of beta-interferon on gamma-interferon production could have triggered a preferential expansion of Th2 type T-helper cells whose particular profile of cytokine secretion has been shown to play a crucial role in the development of eosinophilia. To the authors' knowledge, this is the first report of eosinophilia induced by beta-interferon therapy for chronic hepatitis C.

Chronic Disease↗

PubMed2004

Primary biliary cirrhosis presented as peripheral eosinophilia in asymptomatic women with or without elevated alkaline phosphatase.

Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease characterized by the destruction of biliary epithelial cells, presumably by autoimmune mechanism(s). Although lymphocytes play a pivotal role in the pathogenesis of PBC, the possible involvement of eosinophils has also been suggested. Recent studies have shown that eosinophilia possibly occurs in the peripheral blood of PBC patients. We present four cases of asymptomatic middle-aged women with moderate-to-high eosinophilia observed during random investigation. Alkaline phosphatase (ALP) was increased in two of them. As a result of clinical and laboratory evaluations the early stages of PBC were diagnosed in all the patients, as attested by the detection of high titres of anti-mitochondrial antibodies and the characteristic lesions on liver biopsies. Liver function tests and eosinophils returned within normal limits after 2 months of treatment with ursodeoxycholic acid, suggesting that its potential immunomodulatory actions may extend to eosinophils. Our report further supports the possibility that eosinophilia may occur in PBC, especially in its early stages. From the clinical point of view, we believe that PBC should be considered in the differential diagnosis of eosinophilia with an otherwise unknown origin. In particular, PBC should be suspected in a patient when other causes of eosinophilia have been excluded, irrespective of the presence or absence of symptoms, or the presence or absence of elevated ALP. In such cases further evaluation for anti-mitochondrial antibodies should be done. These observations might assist the development of future therapeutic concepts in the management of PBC, at least for patients in early stages of the disease.

Adult↗

PubMed1996

The pulmonary infiltration with eosinophilia syndrome.

The term eosinophilia denotes an absolute eosinophil count above 500 cells/microL. Eosinophilia has been noted in various inflammatory disorders: skin conditions (eczema, dermatitis, generalized drug reactions), malignancies (Hodgkin's disease and lung cancer), chronic granulomatous disorders (tuberculosis, sarcoidosis), fungal diseases (coccidioidomycosis, aspergillosis), drug- and chemical--related conditions, and idiopathic pulmonary infiltrate and eosinophilia syndromes. The incidence of pulmonary infiltration with eosinophilia is on the rise. Idiopathic pulmonary eosinophilia should be distinguished from the eosinophilic myeloproliferative syndrome. The diagnosis can usually be secured with the help of a good history and physical examination enhanced by simple laboratory tests on blood and sputum and a chest radiogram. The therapy is then directed to correct the initial injury.

Diagnosis, Differential↗

PubMed1994

Serum levels of major basic protein in patients with or without eosinophilia: measurement by enzyme-linked immunosorbent assay.

A bone marrow proteoglycan (BMPG) has been purified which consists of the same amino acid sequence as that of pro-MBP, and produced two anti-BMPG mAbs. Serum levels of major basic protein (MBP), a cationic protein rich in the eosinophil granule, were measured in patients with eosinophilia or allergic diseases by an enzyme-linked immunosorbent assay (ELISA) using these mAbs. The serum levels of MBP in patients with eosinophilia (n = 64) and in those with allergic diseases without eosinophilia (n = 32) were elevated significantly (P < 0.001 and P = 0.038, respectively). There was a weak positive correlation between the serum levels of MBP and the eosinophil counts in the patients with eosinophilia (r = 0.38). Among these patients, extremely high serum levels of MBP were found in those with hypereosinophilic syndrome (HES) and Kimura's disease. Serum levels of MBP decreased more slowly than the eosinophil counts in patients with eosinophilia when treated by glucocorticoids. We conclude that measurement of serum levels of MBP is useful in evaluating the total-body proliferation and infiltration of eosinophils more accurately than following-up the eosinophil counts alone.

Aged↗

PubMed2004

Eosinophilia in nasal polyposis: its objective quantification and clinical relevance.

BACKGROUND: Eosinophilia within nasal polyps is often taken as a criterion for adjuvant medical treatment postoperatively such as topical steroids. OBJECTIVE: This study was performed in order to validate a new technique for objective quantification of eosinophilia by using laser scanning cytometry (LSC), to compare these results with manual scoring and routine histopathology, and to correlate them with the history of allergy or recurrence. METHODS: LSC was used for semi-automated analysis of single-cell preparations from representative ethmoidal polyps obtained during routine paranasal sinus surgery (n=41). This microscope-based instrument scans the cells after immobilization of cells on a glass slide and after triple staining of cytokeratin, eosinophilic granula, and DNA. The location of each cell is stored with the fluorescence data. Therefore, the morphology of every cell can be documented by re-staining with haemotoxylin and eosin and re-localization on the slide. Subsequently, slides were subjected to manual scoring. The remaining polyps were analysed by routine histopathology. RESULTS: Data from LSC and manual scoring showed good correlation (r=0.81, P<0.001), whereas there were discrepancies with histopathology. Eosinophilia scored by LSC and histopathology was neither correlated with the history of allergy nor with recurrence as determined by Fisher's exact test independent of the definition of eosinophilia (> or =2%, > or =3%, or > or =5% of all cells). CONCLUSION: Scoring eosinophilia by LSC in comparison with histopathology does not contribute to a more reliable basis for adjuvant medical therapy in nasal polyposis. Instead, functional parameters (cytokine production, apoptosis) may serve better.

Eosinophilia↗

PubMed1992

Protective effects of cyclophosphamide, cyclosporin A and FK506 against antigen-induced lung eosinophilia in guinea-pigs.

A close association has been recognized between activated T cells and eosinophils in asthma, albeit circumstantial. The present study attempted to investigate this relationship in an animal model of lung eosinophilia using the new generation of T cell-selective immunosuppressants, cyclosporin A and FK506, compared with the myelotoxic immunosuppressive agent cyclophosphamide. Antigen challenge of ovalbumin-sensitized guinea-pigs resulted in a lung eosinophilia which was assessed by bronchoalveolar lavage. All three agents caused a marked suppression of lung eosinophilia at 24 h post-challenge when the compounds were administered at the time of sensitization but not when administered for 3 days before lavage. However, the lung eosinophilia at 72 h post-challenge was reduced significantly by FK506 and by cyclophosphamide, but not by cyclosporin A, when the drugs were administered for 3 days, before lavage. These results strongly suggest the involvement of T cells in antigen-induced late phase (72 h) eosinophilia in guinea-pigs but not at 24 h. The effects of cyclophosphamide were always associated with a reduction in circulating white cell counts, whereas cyclosporin A and FK506 showed no myelotoxic properties. These results suggest the potential therapeutic use of selective, non-cytotoxic immunosuppressive agents in asthma.

Animals↗

PubMed1985

Induction of a marked eosinophilia by cyclophosphamide in Toxocara canis infected SJL mice.

Cyclophosphamide (Cy) is known to produce a marked eosinophilia in mice after antigen challenge. In this study, we studied the effect of Cy on eosinophilia in helminthic infection. Peripheral blood eosinophils were counted in SJL mice following a large dose of Cy injection, infection with Toxocara canis, and both Cy injection and T. canis infection simultaneously. Following the injection with Cy (150 mg/kg), the eosinophil counts fell sharply, then rose abruptly to six times the normal level followed by a decrease. Infection with T. canis induced eosinophilia in mice. However, when mice were both infected with T. canis and given Cy injection, the eosinophilia was markedly enhanced. The results suggest that the marked eosinophilia in mice induced by Cy is not only observed in antigen challenge but also in helminthic infection.

Animals↗

PubMed2005

Additive effect of eosinophilia and atopy on exhaled nitric oxide levels in children with or without a history of respiratory symptoms.

Although atopy and blood eosinophilia both influence exhaled nitric oxide (eNO) measurements, no study has quantified their single or combined effect. We assessed the combined effect of atopy and blood eosinophilia on eNO in unselected schoolchildren. In 356 schoolchildren (boys/girls: 168/188) aged 9.0-11.5 yr, we determined eNO, total serum IgE, blood eosinophil counts and did skin prick tests (SPT) and spirometry. Parents completed a questionnaire on their children's current or past respiratory symptoms. Atopy was defined by a SPT >3 mm and eosinophilia by a blood cell count above the 80th percentile (>310 cells/ml). eNO levels were about twofold higher in atopic-eosinophilic subjects than in atopic subjects with low blood eosinophils [24.3 p.p.b. (parts per billion) vs. 14.1 p.p.b.] and than non-atopic subjects with high or low blood eosinophils (24.3 p.p.b. vs. 12.2 p.p.b. and 10.9 p.p.b.) (p <0.001 for both comparisons). The additive effect of atopy and high eosinophil count on eNO levels remained unchanged when subjects were analyzed separately by sex or by a positive history of wheeze (n=60), respiratory symptoms other than wheeze (n=107) or without respiratory symptoms (n=189). The frequency of sensitization to Dermatophagoides (Dpt or Dpf) was similar in atopic children with and without eosinophilia (66.2% and 67.4%, respectively); eosinophilia significantly increased eNO levels in Dp-sensitized children as well in children sensitized to other allergens. In a multiple linear regression analysis, eNO levels were mainly explained by the sum of positive SPT wheals and a high blood eosinophil count (t=4.8 and 4.3, p=0.000), but also by the presence of respiratory symptoms (especially wheeze) and male sex (t=2.6 and 2.0, p=0.009 and 0.045, respectively). Measuring eNO could be a simple, non-invasive method for identifying subjects at risk of asthma in unselected school populations.

Analysis of Variance↗

PubMed2006

Prevalence of allergic rhinitis and nasal smear eosinophilia in 11- to 15 yr-old children in Shiraz.

Allergic rhinitis (AR) is a common condition among schoolchildren. The prevalence rate of AR differs among countries and even among regions within the same country. The objective of this study was to determine the prevalence of nasal symptoms and signs of AR and nasal smear eosinophilia in 11- to 15-yr-old children in Shiraz. A total of 4584 children aged 11-15 yr of both sexes were surveyed from May 1995 to April 1996, and nasal symptoms and signs of AR (sneezing, rhinorrhea, nasal blockage, itching, color change, mucosal swelling, nasal wetness, and nasal crease), based on questionnaire and ear, nose and throat (ENT) examination were recorded. In addition, smears were taken from nasal secretions and stained. The results compared with nasal smears related to 340 healthy children. 1008 (22%) schoolchildren had nasal symptoms of AR (based on the questionnaire), 445 (9.7%) were identified as having nasal symptoms and signs of AR (based on the questionnaire and ENT specialist examination), and 226 (5.8%) had nasal symptoms and signs of AR associated with nasal eosinophilia (based on the questionnaire, ENT specialist examination and positive nasal smear for eosinophilia). Nasal eosinophilia was present in 274 (62%) children with nasal symptoms and signs of AR. This survey showed that prevalence of nasal symptoms and signs of AR was high in schoolchildren in Shiraz. Nasal smear eosinophilia had a diagnostic specificity of 96% and sensitivity of 62% and seems to be a potentially valuable test for AR.

Adolescent↗

PubMed1988

Carcinoma of the cervix with massive eosinophilia.

Massive local eosinophilia of 100 or more eosinophils per high power field was found in 3.2% cases of invasive carcinoma of the cervix. The prevalence, length of history before presentation to surgery and histological features were similar in patients from Great Britain and Malawi, but in both populations the mean age at diagnosis was lower than in patients with cervical carcinomas without tissue eosinophilia. In some of the tumours, the malignant cells were very difficult to find because of the eosinophil infiltrate, and misinterpretation as an inflammatory lesion was possible. In the absence of circulating eosinophilia, cervical carcinomas with massive eosinophilia were found to have a better prognosis than tumours without. Five patients had circulating eosinophilia as well as local tumour eosinophil infiltration, and each of them had extensive tumour spread.

Adult↗

PubMed1992

Conjunctival eosinophilia in atopic and non-atopic external eye symptoms.

We studied the occurrence in an ophthalmological office practice of conjunctival eosinophilia in 333 normal subjects (mean age 26 years) and in 152 atopic and 484 non-atopic patients (mean age 40 years) with various external eye symptoms. Eosinophils were present in 131/636 patients (21%) and in 22/333 asymptomatic normal subjects (7%). In those patients with conjunctival eosinophilia, a history of some kind of atopic condition was obtained only in 53/131 (40%). When the patients were characterized according to the presence of both eosinophilia and atopy, eosinophilia without signs of atopy was observed in 7-15% in different diagnostic groups. Patients with conjunctivitis or blepharoconjunctivitis had a fourfold risk for eosinophilia compared to normal subjects (odds ratios 4.52 and 4.09, confidence intervals 2.02, 10.12 and 2.40, 6.99), when atopy, sex, age, time of the examination and presence of bacteria were included as potential confounders in the regression model. We conclude that a considerable portion of patients with external eye symptoms, and especially with various forms of conjunctivitis, show eosinophilic inflammation without any evidence of atopic background. They can be labelled as having 'intrinsic' eosinophilic conjunctivitis analogously to the classification used in patients with intrinsic rhinitis and asthma. The etiology of this common nonatopic syndrome remains to be established.

Adolescent↗

PubMed1999

Secreted respiratory syncytial virus G glycoprotein induces interleukin-5 (IL-5), IL-13, and eosinophilia by an IL-4-independent mechanism.

The attachment glycoprotein G of respiratory syncytial virus (RSV) is produced as both membrane-anchored and secreted forms by infected cells. Immunization with secreted RSV G (Gs) or formalin-inactivated alumprecipitated RSV (FI-RSV) predisposes mice to immune responses involving a Th2 cell phenotype which results in more severe illness and pathology, decreased viral clearance, and increased pulmonary eosinophilia upon subsequent RSV challenge. These responses are associated with increased interleukin-4 (IL-4) production in FI-RSV-primed mice, and the responses are IL-4 dependent. RNase protection assays demonstrated that similar levels of IL-4 mRNA were induced after RSV challenge in mice primed with vaccinia virus expressing Gs (vvGs) or a construct expressing only membrane-anchored G (vvGr). However, upon RSV challenge, vvGs-primed mice produced significantly greater levels of IL-5 and IL-13 mRNA and protein than vvGr-primed mice. Administration of neutralizing anti-IL-4 antibody 11.B11 during vaccinia virus priming did not alter the levels of vvGs-induced IL-5, IL-13, pulmonary eosinophilia, illness, or RSV titers upon RSV challenge, although immunoglobulin G (IgG) isotype profiles revealed that more IgG2a was produced. vvGs-priming of IL-4-deficient mice demonstrated that G-induced airway eosinophilia was not dependent on IL-4. In contrast, airway eosinophilia induced by FI-RSV priming was significantly reduced in IL-4-deficient mice. Thus we conclude that, in contrast to FI-RSV, the secreted form of RSV G can directly induce IL-5 and IL-13, producing pulmonary eosinophilia and enhanced illness in RSV-challenged mice by an IL-4-independent mechanism.

Animals↗