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PubMed2004

STAT6-mediated signaling in Th2-dependent allergic asthma: critical role for the development of eosinophilia, airway hyper-responsiveness and mucus hypersecretion, distinct from its role in Th2 differentiation.

When wild-type BALB/c mice were transferred with OVA-specific Th2 cells followed by OVA inhalation, a severe eosinophilia, mucus hypersecretion and airway hyper-responsiveness (AHR) was induced in parallel with a marked elevation of IL-4, IL-5 and IL-13 levels in bronchoalveolar lavage fluid (BALF). However, neither eosinophilia, AHR nor mucus hypersecretion was induced in Th2 cell-transferred STAT6-/- mice. The failure of eosinophilia was not due to the defect of Th2 cytokine production in BALF of STAT6-/- mice transferred with Th2 cells, but because of the defect of STAT6-dependent eotaxin production. Indeed, intranasal administration of eotaxin reconstituted pulmonary eosinophilia but not AHR and mucus hypersecretion in OVA-inhalated STAT6-/- mice. These results initially provided direct evidence that STAT6-dependent eotaxin production is essential for pulmonary eosinophilia. We also dissociated the role of STAT6 for eosinophilia from that for AHR and mucus hypersecretion. Thus, STAT6 also plays a critical role at late phase of Th2-dependent allergy induction.

Administration, Intranasal↗

PubMed2005

Allergic airway eosinophilia is suppressed in ovalbumin-sensitized Brown Norway rats fed raffinose and alpha-linked galactooligosaccharide.

We recently found that dietary raffinose suppressed allergic airway eosinophilia in ovalbumin-sensitized Brown Norway rats. Using this model in the present study, we compared the efficacy of other oligosaccharides with that of raffinose. Brown Norway rats were immunized s.c. with ovalbumin on d 0 and exposed to aerosolized ovalbumin on d 20; broncho-alveolar lavage fluid was obtained on d 21. In Expt. 1, rats were fed a control diet or diets supplemented with different oligosaccharides (50 g/kg diet, raffinose, alpha-linked galactooligosaccharide, fructooligosaccharide, and xylooligosaccharide). The number of eosinophils in the fluid was significantly lower in rats fed raffinose and alpha-linked galactooligosaccharide diets than in those fed the control diet. Dietary fructooligosaccharide and xylooligosaccharide did not affect airway eosinophilia. In Expt. 2, i.p. administration of raffinose and alpha-linked galactooligosaccharide, but not fructooligosaccharide and xylooligosaccharide, suppressed airway eosinophilia in rats fed the control diet. In Expt. 3, suppression of airway eosinophilia by dietary alpha-linked galactooligosaccharide occurred in cecectomized rats administered neomycin. Reduced levels of interleukin (IL)-4 and IL-5 mRNA in lung tissue were associated with the suppression of airway eosinophilia. We propose that indigestible oligosaccharides differ in their suppressive effect on allergic airway eosinophilia in ovalbumin-sensitized Brown Norway rats and that the effect appears not to be mediated by intestinal microflora.

Animals↗

PubMed1998

Successful challenge with clozapine in a history of eosinophilia.

Eosinophilia has been encountered from 0.2 to 61.7% in clozapine-treated patients, mostly with a transient course and spontaneous remission. There have been few reports, however, which have investigated a challenge with clozapine in patients previously showing eosinophilia. Two case reports are presented: the first with clozapine challenge after eosinophilia, the second under clozapine treatment and no previous haematological side effects. The challenge case showed eosinophilia with 1.2 10(9)/l (z = 1.79, p = 0.04) being followed by normalization despite clozapine continuation, whereas the maximum value reached 2.1 10(9)/l in the single episode case, with consecutive normalization and uninterrupted treatment. Eosinophilia caused by clozapine was observed in challenge, preceded by a faster neutrophil production and consecutive decrease (z = 2.27, p = 0.01). A challenge with clozapine was feasible and showed no clinical symptoms of eosinophilia.

Adolescent↗

PubMed2003

Esophageal eosinophilia in children with dysphagia.

OBJECTIVES: Children occasionally have dysphagia in the absence of an apparent primary cause. Esophageal eosinophilia is sometimes seen in these patients at the time of upper endoscopy but its significance is not clear. Although eosinophilia is regarded by some as a histologic hallmark of childhood reflux esophagitis, it may in fact signal a primary eosinophilic esophagitis in children with dysphagia. Our aim was to evaluate esophagitis, acid reflux determined by pH probe, and esophageal eosinophilia in children with the primary complaint of dysphagia. METHODS: A retrospective study was performed in 42 children, admitted for investigation of dysphagia, in whom no primary cause could be found. Twenty-one children (mean age +/- SD, 10.1 +/- 4.0 years) had esophageal eosinophilia and 21 children (8.3 +/- 4.7 years) did not. Clinical, endoscopic, manometric and esophageal pH parameters in these two groups were compared. RESULTS: Patients with esophageal eosinophilia were more often male (p<0.01) with a history of allergy (p<0.001) and food bolus obstruction (p<0.05) requiring endoscopic removal. Their esophageal mucosa appeared wrinkled and thickened at endoscopy with basal cell proliferation, and large numbers of eosinophils in esophageal mucosal biopsies. Continuous esophageal pH records and motility studies, when obtained, were similar in both groups and were within normal values. CONCLUSION: Children with dysphagia who have esophageal eosinophilia are unlikely to have pathologic gastroesophageal reflux.

Adolescent↗

PubMed2006

Kimura's disease and angiolymphoid hyperplasia with eosinophilia: two disease entities in the same patient: case report and review of the literature.

BACKGROUND: Much controversy has existed with regard to the relationship between Kimura's disease and angiolymphoid hyperplasia with eosinophilia. They were initially thought to represent the same disease spectrum, but it has now been widely accepted that they are two separate disease entities. To our knowledge, there have been no reports to date describing a case of both Kimura's disease and angiolymphoid hyperplasia with eosinophilia coexisting in the same patient. METHODS: We describe a patient presenting initially with a right postauricular subcutaneous swelling and subsequently developing multiple erythematous facial papules and nodules. The medical literature is reviewed. RESULTS: Clinical features of the right postauricular subcutaneous swelling and multiple erythematous facial papules/nodules suggest Kimura's disease in the former and angiolymphoid hyperplasia with eosinophilia in the latter. Histopathological examinations of these lesions helped to confirm the diagnosis of Kimura's disease and angiolymphoid hyperplasia with eosinophilia, respectively. CONCLUSIONS: Kimura's disease and angiolymphoid hyperplasia with eosinophilia can coexist in the same patient. Coexistence of the two types of lesions in one patient may also be considered evidence that Kimura's disease and angiolymphoid hyperplasia with eosinophilia form a spectrum in one disease.

Adrenal Cortex Hormones↗

PubMed1987

Selective peripheral blood eosinophilia associated with survival advantage in Hodgkin's disease (BNLI Report No 31). British National Lymphoma Investigation.

A peripheral blood eosinophilia was found at presentation in 193 of 1260 (15%) patients with Hodgkin's disease who had been entered into clinical studies by the British National Lymphoma Investigation (BNLI). Eosinophilia as a component of a general leucocytosis conferred no survival advantage. Eosinophilia without a general leucocytosis was present in 95 patients, and this selective eosinophilia was associated with a clear survival advantage. The association of selective eosinophilia and improved survival was limited to patients with mixed cellularity and grade I nodular sclerosis histology. Selective eosinophilia was found to be a good prognostic indicator both in local and generalised disease. Its survival advantage seemed to lie in the response to second line treatment following relapse.

Eosinophilia↗

PubMed2001

Eotaxin-1-deficient mice develop airway eosinophilia and airway hyperresponsiveness.

BACKGROUND: The accumulation of eosinophils in the lung is a hallmark of asthma. In addition to cytokines such as IL-5 which are essential, chemokines have been implicated in the recruitment of eosinophils to the airway. In particular, eotaxin has been shown to be a selective and potent eosinophil chemoattractant, important in the pathogenesis of allergic disease. The goal of the present study was to define the role of eotaxin-1 in the development of allergen-induced eosinophilic airway inflammation and airway hyperresponsiveness (AHR) to inhaled methacholine (MCh). METHODS: Eotaxin-1-deficient mice were sensitized and exposed to a single challenge with allergen. Airway function and airway and tissue as well as peripheral blood and bone marrow eosinophilia were examined 18 and 48 h after the last challenge. RESULTS: Following allergen sensitization and challenge, eotaxin-1-deficient mice developed levels of AHR to inhaled MCh at 18 and 48 h comparable to controls. Further, levels of bronchoalveolar lavage (BAL) and tissue eosinophilia at the same time points were comparable in the two strains of mice. Tissue eosinophilia, assessed by quantitating major basic protein staining cells, preceded BAL eosinophilia in a similar manner. Bone marrow and peripheral blood eosinophilia were unimpaired in deficient mice. CONCLUSION: The results demonstrate that the major eotaxin, eotaxin-1 is not essential for the development of airway eosinophilia or AHR, implying that other chemokines, alone or in combination, can overcome this deficiency.

Allergens↗

PubMed2001

Expression of VLA-4 on eosinophils decreases in patients with eosinophilia.

BACKGROUND: It is assumed that the very late antigen-4 (VLA-4) plays a key role in selective migration and accumulation of eosinophils to the allergic inflammatory focus. The regulatory mechanism for VLA-4 expression is poorly understood, as is its relationship between other adhesion molecules. OBJECTIVE: The aim of the study was to elucidate the relationship between VLA-4 expression and the activation of eosinophils. METHODS: The surface expression of VLA-4, Mac-1, ICAM-1, CD4, CD25, CD69, CD89, IL-5 receptor and GM-CSF receptor on eosinophils isolated from the peripheral blood of 15 patients with eosinophilia and 16 healthy volunteers was measured. RESULTS: The surface expression of VLA-4 presented in mean fluorescent intensity by flow-cytometric analysis showed a significant decrease in the patients with eosinophilia (>700 eosinophils/microl) compared to that of the subjects without eosinophilia. On the other hand, the surface expression of Mac-1 was significantly increased in the patients with eosinophilia. There was an inverse correlation between the expression of VLA-4 and that of Mac-1 (r = -0.81) on the eosinophils obtained from the patients with eosinophilia. CONCLUSION: The changes on the surface expressions of Mac-1 and VLA-4 may be indicating the activation of eosinophils in the patients with eosinophilia and may contribute to their migration to the allergic inflammatory focus.

Adult↗

PubMed1987

Inhibitory immunization using complete Freund's adjuvant on ongoing eosinophilia induced by repeated antigen-stimulations in guinea pigs.

Ongoing eosinophilia, in guinea pigs repeatedly sensitized with dinitrophenylated (DNP)-Ascaris antigen (DNP-Asc) into the peritoneal cavity, was suppressed significantly by complementary immunizations with a heterologous antigen, e.g., ovalbumin (OA) or bovine gamma-globulin (BGG) emulsified in complete Freund's adjuvant (CFA). Challenge injections of DNP-OA or DNP-BGG elicited peritoneal eosinophilia in animals that were sensitized repeatedly with DNP-Asc. Under these conditions, antigen specificity in suppressive immunization was studied. Eosinophilia, induced by DNP-OA challenge, was suppressed by immunization with either OA in CFA or BGG in CFA. However, Asc (homologous carrier of sensitizing antigen) elicited no suppression. Additionally, CFA, used as an adjuvant, played an important role in suppressive immunization, but CFA alone had no effect in suppressing peritoneal eosinophilia. Anti-DNP antibody, detected by hemagglutination test or passive cutaneous anaphylaxis, was not affected by complementary immunization. These results suggested that peritoneal eosinophilia was suppressed concomitantly by a supplemental immunization in an antigen-nonspecific manner. Eosinophilia in the bone marrow also was suppressed significantly by complementary immunization, but the pattern was quite different from that shown in the peritoneal cavity. The first nuclear cell response peak after challenging, including eosinophils, was stanched completely by CFA itself. The second nuclear cell peak, on day 5, recovered, but eosinophil response continued to be suppressed.

Animals↗

PubMed1999

TRFK-5 reverses established airway eosinophilia but not established hyperresponsiveness in a murine model of chronic asthma.

We studied the effects of an anti-interleukin (IL)-5 monoclonal antibody (TRFK-5) or dexamethasone (DEX) to reverse already established airway hyperresponsiveness (AHR) and tissue eosinophilia in a Schistosoma mansoni antigen-sensitized and airway-challenged mouse model of chronic asthma. In this model at 4 d after antigen challenge there is dramatic bronchoalveolar lavage fluid (BAL) eosinophilia, AHR to intravenous methacholine (MCh), and histologic evidence of peribronchial eosinophilic infiltration and mucoid cell hyperplasia. These changes persist for up to 2 wk after antigen challenge. Treatment with DEX from Days 4 through 10 significantly reduced established airway eosinophilia compared with animals sham-treated with saline from Days 4 -10 (120 +/- 29 eosinophils/microl BAL for DEX-treated mice versus 382 +/- 60 eosinophils/microl BAL for sham-treated animals, p < 0.01). DEX-treated mice also had dramatically reduced mucoid cell hyperplasia, and airway responsiveness returned to normal. In contrast, TRFK-5 given during the same time period reduced airway eosinophilia (86 +/- 32 eosinophils/microl BAL versus 382 +/- 60 eosinophils/microl BAL, p < 0.01) but did not reduce goblet cell hyperplasia or reverse already established AHR. Treatment with DEX but not TRFK-5 also inhibited interferon gamma (IFN-gamma) content of BAL fluid (0.49 +/- 0.09 ng/ml BAL fluid for DEX versus 1.50 +/- 0.24 ng/ml BAL fluid and 1.36 +/- 0.13 ng/ml BAL fluid for TRFK-5 and sham-treated mice, respectively, both p < 0.001 versus DEX). Thus, treatment with DEX reduces established eosinophilic airway inflammation and AHR in S. mansoni-sensitized and airway-challenged mice but treatment with TRFK-5 reversed established eosinophilia without ameliorating established AHR. Together, these data suggest that once airway inflammation develops, neutralizing the effects of IL-5 or reducing eosinophilia alone may not result in inhibiting established AHR in atopic asthma.

Allergens↗

PubMed1991

Blood eosinophilia and FEV1. Cross-sectional and longitudinal analyses.

A previous cross-sectional analysis of 1980 data from a population of working men in the Paris area has shown a significant relationship of blood eosinophilia to a reduced FEV1 among nonsmokers, remaining after excluding men with a history of asthma. In the present report, we reexamine this relationship, after taking into account asthma, bronchial hyperresponsiveness, and positive skin prick tests, using data collected in 1985 in a subsample of 363 men from the initial population. Blood eosinophilia, defined by 5% or more eosinophils or by 250 or more eosinophils per cubic millimeter appeared to be associated with a lower FEV1, primarily in nonsmokers. A difference of approximately 0.40 L was observed in never-smokers with eosinophilia (greater than or equal to 5% of eosinophils) compared with those without. This association persisted after exclusion of subjects with atopy, asthma, and bronchial hyperresponsiveness. Longitudinally, no significant association was observed between 1980 eosinophilia and the annual FEV1 decline between 1980 and 1985, even in nonsmokers. The results of our cross-sectional analyses suggest that asthma or asthma-like disorder does not explain the association between eosinophilia and FEV1. The role of eosinophil in respiratory disorders may go beyond its intervention in allergy. Further longitudinal studies are needed to better understand discrepancies between cross-sectional and longitudinal data and whether eosinophilia is a risk factor for chronic air-flow limitation.

Adult↗

PubMed2003

Involvement of the cysteinyl-leukotrienes in allergen-induced airway eosinophilia and hyperresponsiveness in the mouse.

The leukotriene modifiers are a novel generation of therapeutic agents in the treatment of allergic asthma. However, the mechanisms by which the cysteinyl (cys) leukotrienes (LTs) participate in allergen-induced airway eosinophilia and airway hyperresponsiveness (AHR) are still unclear. In the present study, we have investigated the role of cys-LTs in ovalbumin (OVA)-induced airway responses in a murine model of asthma. Montelukast (3 or 10 mg/kg), a selective cys-LT1 receptor antagonist, reduced airway eosinophilia and AHR after OVA challenge. The levels of interleukin (IL)-5 and eotaxin in the bronchoalveolar lavage fluid (BALF) from montelukast-treated (3 mg/kg) mice were unaffected, although a decrease in IL-5 was observed with a dose of 10 mg/kg. LTD4 (50 ng) instilled intranasally to immunized mice augmented macrophages in the BALF, but in conjunction with OVA challenge it caused BALF eosinophilia and neutrophilia when given before challenge and BALF neutrophilia but not eosinophilia when given 2 h after challenge. However, there were no increases of IL-5 or eotaxin in BALF following LTD4 treatment. Repeated instillations of LTD4 to immunized mice, mimicking allergen challenge, did not induce AHR but in conjunction with OVA challenge LTD4 enhanced AHR. These results indicate that allergen-induced eosinophilia and AHR are in part mediated by the cys-LT1 receptor, and that, although LTD4 alone has no effect on airway eosinophilia, in conjunction with antigenic stimulation it potentiates the degree of airway inflammation and AHR.

Acetates↗

PubMed1997

Relationship between interleukin-5 and eotaxin in regulating blood and tissue eosinophilia in mice.

The mechanism of cooperation between IL-5 and eotaxin for the selective accumulation of eosinophils at sites of allergic inflammation is unknown. In this investigation we have used IL-5 deficient mice to define the relationship between this cytokine and eotaxin in the regulation of blood eosinophilia and eosinophil homing and tissue accumulation. Both IL-5 and eotaxin could independently induce a rapid and pronounced blood eosinophilia in wild type mice when administered systemically. In contrast, only eotaxin induced a pronounced blood eosinophilia in IL-5 deficient mice. The eosinophilic response induced by intravenous eotaxin in wild type mice did not correlate with a significant reduction in the level of bone marrow eosinophils, whereas intravenous IL-5 resulted in depletion of this store. These results suggest the existence of two mechanisms by which eosinophils can be rapidly mobilized in response to intravenous eosinophil chemoattractants; first, mobilization of an IL-5 dependent bone marrow pool, and second, an eotaxin-induced sequestration of eosinophils from tissues into the blood. Subcutaneous injection of eotaxin induced a local tissue eosinophilia in wild type mice but not in IL-5 deficient mice. Furthermore, tissue eosinophilia in wild type mice, but not in IL-5 deficient mice, was enhanced by adoptive transfer of eosinophils or the administration of intravenous IL-5. However, pretreatment of IL-5 deficient mice with intraperitoneal IL-5 for 72 h restored eosinophil homing and tissue accumulation in response to subcutaneous eotaxin. We propose that eotaxin secreted from inflamed tissue may play an important role in initiating both blood and tissue eosinophilia in the early phases of allergic inflammation. Furthermore, IL-5 is not only essential for mobilizing eosinophils from the bone marrow during allergic inflammation, but also plays a critical role in regulating eosinophil homing and migration into tissues in response to eotaxin and possibly other specific chemotactic stimuli.

Adoptive Transfer↗

PubMed2005

Valproate-induced eosinophilia in children with epilepsy: role of interleukin-5.

Interleukin-5 contributes both in eosinophilopoiesis and neural development. Serum interleukin-5 levels were measured with enzyme-linked immunosorbent assay technique in 68 children with epilepsy receiving sodium valproate monotherapy and compared with the levels of 60 healthy controls and 14 children with epilepsy receiving carbamazepine. Eosinophilia was observed in 35.3% of children receiving valproate. Interleukin-5 in valproate users was significantly higher compared with children receiving carbamazepine and controls. Valproate users who exhibited eosinophilia had higher interleukin-5 levels compared with those without eosinophilia. However, the interleukin-5 level was also elevated, although to a lesser degree, in children without eosinophilia. The majority of valproate responders had high interleukin-5 levels. A positive correlation between interleukin-5 levels and the eosinophil count was also noted. We postulate that valproate contributes to the pathogenesis of eosinophilia, probably inducing interleukin-5 production. The finding that serum interleukin-5 was significantly elevated in valproate responders and even in valproate users without eosinophilia suggests that the increase in interleukin-5 might represent one of valproate's antiepileptic mechanisms.

Adolescent↗

PubMed1995

Eosinophilia associated with bupropion.

OBJECTIVE: To describe the first incidence of eosinophilia following administration of bupropion. CASE SUMMARY: The patient was a 72-year-old woman admitted for evaluation of chest pain. During hospitalization, the eosinophil count reached 0.60 fraction of 1.00, with absolute eosinophil count of 6693 x 10(6)/L and a white blood cell count of 18.5 x 10(9)/L. She had been receiving bupropion therapy for 5 days prior to this admission. DISCUSSION: Potential causes of the eosinophilia, including disease states and medications, were reviewed comprehensively and ruled out. A review of the literature (MEDLINE 1966-1994) did not identify previous cases of eosinophilia associated with bupropion therapy. Causes of eosinophilia include parasitic infections, allergic diseases, and medication use. A proposed mechanism for the occurrence of eosinophilia in this patient is unknown. CONCLUSIONS: Considering the temporal sequence of events, drugs administered prior to the development of eosinophilia, and the rapid decline of the eosinophil count following discontinuation of the medication, bupropion appears to be the precipitating agent.

Aged↗

PubMedDate not supplied

Eosinophilia-myalgia syndrome: the Cleveland Clinic experience.

Eosinophilia-myalgia syndrome is a recently described clinical syndrome caused by a suspected contaminant of L-tryptophan, an essential amino acid that was manufactured and sold as a nutritional supplement. This study reports the clinical and pathological findings of 22 cases of eosinophilia-myalgia syndrome evaluated at the Cleveland Clinic and includes data for up to 1 year of follow-up (for the epidemic cases). Nineteen of the 22 cases were evaluated and followed prospectively in the time period from November 1989 to November 1990. Two of the 22 represented nonepidemic forms of the syndrome which occurred prior to the 1989 epidemic. During a review of all cases of biopsy-proven diffuse fasciitis with eosinophilia at the Cleveland Clinic since 1978, one of the 22 was retrospectively identified as having an epidemic form of the syndrome, with onset in July 1989. In this study, adverse prognosticating factors in eosinophilia-myalgia syndrome included nerve and muscle involvement, fasciitis, and weight loss. Eosinophilia-myalgia syndrome is striking in its severity and diversity, and its features are similar to those of two other unusual illnesses--toxic oil syndrome and diffuse fasciitis with eosinophilia. With the recent purification of the suspected contaminant, it is hoped that further clues to the etiology of this syndrome and similar syndromes will be uncovered.

Adult↗

PubMed2002

Chronic exposure to innocuous antigen in sensitized mice leads to suppressed airway eosinophilia that is reversed by granulocyte macrophage colony-stimulating factor.

In this study we investigated the impact of chronic allergen exposure on airway inflammation and humoral responses in sensitized mice. We observed marked eosinophilia in the bronchoalveolar lavage, lung tissue, and peripheral blood after 2 wk of exposure. In contrast, eosinophilia was markedly reduced by 3 wk and completely resolved by 4 wk of exposure, despite the continued presence of Ag. Decreases in airway eosinophilia were associated with a robust humoral response. We observed that levels of OVA-specific IgE, IgG1, and IgG2a increased during the course of exposure. To assess whether continuous exposure to Ag impacts the ability of the lung to respond to subsequent Ag challenge, mice were exposed to either 2 or 4 wk of OVA in the context of GM-CSF. All groups were then rested for 28 days and exposed to OVA on three consecutive days. We observed a significant decrease in airway eosinophilia and IL-5 expression in the bronchoalveolar lavage and serum in mice initially exposed to 4 wk of OVA, compared with animals exposed to 2 wk only. However, in both groups expression of B7.2 on dendritic cells as well as CD25, CD69, and T1/ST2 on CD4(+) T cells was enhanced, suggesting immune activation. Delivery of rGM-CSF fully restored airway eosinophilia. This study shows that exposure to innocuous Ag alone does not lead to persistent eosinophilic airway inflammation, but rather to abrogated eosinophilia. This suppression can be reversed by GM-CSF.

Administration, Intranasal↗

PubMed2003

Marked airway eosinophilia prevents development of airway hyper-responsiveness during an allergic response in IL-5 transgenic mice.

Tissue eosinophilia probably plays important roles in the pathophysiology of bronchial asthma and allergic disorders; however, this concept was challenged recently by controversial results in mouse models of bronchial asthma treated with anti-IL-5 Ab and the failure of anti-IL-5 therapy in humans. We have now used a unique model, IL-5 transgenic (TG) mice, to address a fundamental question: is airway eosinophilia beneficial or detrimental in the allergic response? After sensitization and challenge with OVA, IL-5 TG mice showed a marked airway eosinophilia. Surprisingly, these IL-5 TG mice showed lower airway reactivity to methacholine. Immunohistochemical analysis of the lungs revealed a marked peribronchial infiltration of eosinophils, but no eosinophil degranulation. In vitro, mouse eosinophils from peritoneal lavage fluids did not produce superoxide anion, but did produce an anti-inflammatory and fibrotic cytokine, TGF-beta 1. Indeed, the TGF-beta 1 levels in bronchoalveolar lavage fluid specimens from IL-5 TG mice directly correlated with airway eosinophilia (r = 0.755). Furthermore, anti-IL-5 treatment of IL-5 TG mice decreased both airway eosinophilia and TGF-beta 1 levels in bronchoalveolar lavage fluids and increased airway reactivity. Thus, in mice, marked eosinophilia prevents the development of airway hyper-reactivity during an allergic response. Overall, the roles of eosinophils in asthma and in animal models need to be addressed carefully for their potentially detrimental and beneficial effects.

Allergens↗