Blood eosinophil number and activity in relation to lung function in patients with asthma and with eosinophilia

Griffin, Emma; Håkansson, Lena; Formgren, Hans; Jörgensen, Kirsten; Peterson, Christer; Venge, Per

doi:10.1016/0091-6749(91)90014-f

Cited by 140 publications

(70 citation statements)

References 16 publications

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“…Interestingly, the changes in sputum eosinophils, EG2+ cells and methacholine airway hyperresponsiveness were accompanied by an increase in nocturnal asthma symptoms, as well as β 2 -agonist use. These results are in agreement with other studies that have suggested the functional importance of activated eosinophils in asthma [19,20].…”

Section: Discussionsupporting

confidence: 83%

Increases in airway eosinophils and interleukin-5 with minimal bronchoconstriction during repeated low-dose allergen challenge in atopic asthmatics

Sulakvelidze¹,

Inman²,

Rerecich³

et al. 1998

Eur Respir J

101

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Asthma induced by the inhalation of various allergens in the clinical research laboratory, has been a model for studying pathophysiology and pathogenesis of this disease for many years [1][2][3][4]. The inhalation of a specific allergen by asthmatic subjects can cause three types of airway responses [5]: the isolated response, that develops within 10-30 min after allergen challenge; the isolated late response that develops 3-8 h after the challenge; and the dual response, where subjects develop both early and late airway responses. The late response is associated with allergeninduced increases in airway responsiveness [6] and with eosinophilic airway inflammation [7].The doses of allergen usually used to study experimentally induced asthma are of a magnitude that causes an early response of at least a 15% reduction in forced expiratory volume in one second (FEV1) and a late response of at least 20% [5]. A shortcoming of this method is that these doses of allergen may be much higher than those to which patients with asthma are exposed in their natural environments. This shortcoming has been addressed by IHRE and co-workers [8,9], who used airway challenge with a low-dose of allergen. At first, these investigators studied early and late responses after a single challenge with low-dose allergen [8]. Later, they used repeated lowdose allergen challenge and demonstrated a significant increase in airway hyperresponsiveness [9]. However, the role of airway inflammation in causing these changes, as well as the time course of these events, has not been studied previously.The purposes of the present study were: 1) to determine the effects of repeated low-dose allergen challenge on airway inflammation as measured by numbers of eosinophils and metachromatic cells in induced sputum, as well as markers of eosinophil activation and level of the eosinopoietic cytokine IL-5; 2) to evaluate the effects of repeated low-dose allergen challenge on the development of late responses and methacholine airway hyperresponsiveness and to examine the time course of the changes; and 3) to evaluate the effects of repeated low-dose challenge on asthma symptoms and β 2 -agonist use. Increases in airway eosinophils and interleukin-5 with minimal bronchoconstriction during repeated low-dose allergen challenge in atopic asthmatics. I. Sulakvelidze, M.D. Inman, T. Rerecich, P.M. O'Byrne. ©ERS Journals Ltd 1998.ABSTRACT: Repeated low-dose allergen challenge increases airway hyperresponsiveness in atopic asthmatics. However, it is not known whether low-dose allergen challenge increases airway inflammation.Eight atopic asthmatics were enrolled in a controlled, cross-over study to evaluate the effect and time course of repeated low-dose allergen challenge on airway inflammation and hyperresponsiveness. The dose of allergen to reduce forced expiratory volume in one second (FEV1) by approximately 5% was selected in a screening allergen challenge. The subjects then were challenged for five consecutive days with either diluent or the selected low-dose of a...

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Section: Discussionsupporting

confidence: 83%

Increases in airway eosinophils and interleukin-5 with minimal bronchoconstriction during repeated low-dose allergen challenge in atopic asthmatics

Sulakvelidze¹,

Inman²,

Rerecich³

et al. 1998

Eur Respir J

101

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“…Other studies in older subjects have demonstrated increased s-ECP in asthmatic patients compared to those without asthma [12,13,23,24]. Several studies have demonstrated higher s-ECP levels in atopic compared to nonatopic subjects [13,25].…”

Section: Discussionmentioning

confidence: 96%

Eosinophil cationic protein and tidal flow volume loops in children 0-2 years of age

Carlsen¹,

Halvorsen²,

Ahlstedt³

et al. 1995

Eur Respir J

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E Eo os si in no op ph hi il l c ca at ti io on ni ic c p pr ro ot te ei in n a an nd d t ti id da al l f fl lo ow w v vo ol lu um me e l lo oo op ps s i in n c ch hi il ld dr re en n 0 0--2 2 y ye ea ar rs s o of f a ag ge e TFV loops were measured in 79 awake children (mean age 14 months). Minimum two wheezy episodes (mean 3.2) or minimum 4 weeks persistent wheeze were reported in 41 children (cases), whereas the 38 controls had no history of wheeze. Airways responsiveness (change in ratio of time until peak expiratory flow to total expiratory time (tPEF/tE) after inhaled nebulized salbutamol) was measured in 26 cases and 24 controls. Serum ECP and serum myeloperoxidase (s-MPO) were measured in all children.Cases had significantly lower mean tPEF/tE (0.21) than controls (0.33), and higher mean s-ECP (21.9 µg·L -1 ) than controls (14.0 µg·L -1 ). Serum ECP (but not s-MPO) correlated significantly with the percentage change in tPEF/tE from baseline (r=0.7), but not with initial tPEF/tE. Serum ECP increased significantly with increasing immunoglobulin E (IgE), airways responsiveness and eosinophil count, but decreased with increasing age.TFV responsiveness to salbutamol and s-ECP levels correlate strongly, both probably reflecting airways inflammation, and may possibly be valuable prognostic tools in recurrent wheezy infants and toddlers.

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“…In eosinophil-deficient PHIL mice, both mucus hypersecretion and AHR were abolished (5), although these findings were not confirmed in another eosinophil-ablated strain, ⌬dbl GATA mice (6). In addition, several clinical studies found a close correlation between the number of blood or airway eosinophils and the intensity of AHR or airway remodeling in asthmatic patients (7)(8)(9)(10)(11). These findings strongly indicate that eosinophils play a central role in the effector phase of allergic inflammation.…”

mentioning

confidence: 86%

“…The number of total splenic cells and eosinophils was counted 1,3,5,8,12,18, and 24 days after plasmid injection. To clearly distinguish eosinophils from the neutrophils, three different stains were applied: Diff-Quick stain, May-Grün-wald-Giemsa stain, and Eosino (Hansel) stain (30).…”

Section: Preparation Of Spleen Cellsmentioning

confidence: 99%

IL-5-Induced Hypereosinophilia Suppresses the Antigen-Induced Immune Response via a TGF-β-Dependent Mechanism

Nakagome

Dohi

Okunishi

et al. 2007

The Journal of Immunology

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Although eosinophils play an essential role in allergic inflammation, their role has recently been under controversy. Epidemic studies suggest that hypereosinophilia induced by parasite infection could suppress subsequent Ag sensitization, although the mechanism has not been fully clarified. In this study, we investigated whether eosinophils could suppress the Ag-specific immune response in the airway. BALB/c mice were sensitized and airway challenged with OVA. Systemic hypereosinophilia was induced by delivery of an IL-5-producing plasmid. IL-5 gene delivery suppressed the Ag-specific proliferation and cytokine production of CD4+ T cells in the spleen. IL-5 gene delivery before OVA sensitization significantly suppressed airway eosinophilia and hyperresponsiveness provoked by subsequent OVA airway challenge, while delivery during the OVA challenge did not suppress them. This IL-5-induced immune suppression was abolished in eosinophil-ablated mice, suggesting an essential role of eosinophils. IL-5 treatment increased the production of TGF-β1 in the spleen, and we demonstrated that the main cellular source of TGF-β1 production was eosinophils, using eosinophil-ablated mice and depletion study. TGF-β1, but not IL-5 itself, suppressed the Ag-specific immune response of CD4+ T cells in vitro. Furthermore, IL-5 treatment enhanced phosphorylation of Smad2 in CD4+ T cells. Finally, a TGF-β type I receptor kinase inhibitor restored this IL-5-induced immune suppression both in vitro and in vivo. These results suggest that IL-5-induced hypereosinophilia could suppress sensitization to Ag via a TGF-β-dependent mechanism, thus suppressed allergic airway inflammation. Therefore, hypereosinophilia could reveal an immunosuppressive effect in the early stage of Ag-induced immune response.

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Blood eosinophil number and activity in relation to lung function in patients with asthma and with eosinophilia

Cited by 140 publications

References 16 publications

Increases in airway eosinophils and interleukin-5 with minimal bronchoconstriction during repeated low-dose allergen challenge in atopic asthmatics

Increases in airway eosinophils and interleukin-5 with minimal bronchoconstriction during repeated low-dose allergen challenge in atopic asthmatics

Eosinophil cationic protein and tidal flow volume loops in children 0-2 years of age

IL-5-Induced Hypereosinophilia Suppresses the Antigen-Induced Immune Response via a TGF-β-Dependent Mechanism

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