Effect of dexamethasone and endogenous corticosterone on airway hyperresponsiveness and eosinophilia in the mouse

Bie, J. J. De; Hessel, Edith M.; Ark, Ingrid van; Esch, Betty C.A.M. van; Hofman, Gerard A.; Nijkamp, Frans P.; Oosterhout, Antoon J. M. van

doi:10.1111/j.1476-5381.1996.tb16062.x

Cited by 56 publications

(15 citation statements)

References 28 publications

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“…Another characteristic of this animal model is the dominant presence of eosinophils in the BALF [33,34,35], a hallmark of allergic asthma in humans [36]. After treatment with B. breve M-16V, the bronchial influx of both eosinophils and lymphocytes in the BALF was reduced, while this was not observed after treatment with any of the other strains.…”

Section: Discussionmentioning

confidence: 99%

Oral Treatment with Probiotics Reduces Allergic Symptoms in Ovalbumin-Sensitized Mice: A Bacterial Strain Comparative Study

Hougee

Vriesema

Wijering³

et al. 2009

Int Arch Allergy Immunol

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154

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Background/Aim: Evidence demonstrating an important role of the intestinal microbiota in the incidence of allergic disorders has led to the concept of using probiotics as possible antiallergic therapy. This study aimed to select a bacterial strain with the best antiallergic treatment effects from a panel of 6 bacterial strains in a mouse model of ovalbumin(OVA)-allergic asthma. Methods: OVA-sensitized BALB/c mice were orally administered the bacterial strains Bifidobacterium breve M-16V, B. infantis NumRes251, B. animalis NumRes252 and NumRes253, Lactobacillus plantarum NumRes8 and L. rhamnosus NumRes6. After challenge by OVA inhalation in the lungs, the response to methacholine was measured. Pulmonary inflammation was assessed by analyzing bronchoalveolar lavage fluid for the presence of eosinophils, neutrophils, macrophages and lymphocytes and for interleukin 4, interleukin 5, interleukin 10 and interferon-γ. OVA-specific IgE, IgG1 and IgG2a were measured in serum. Next, the effect on acute allergic skin reaction was measured after treatment with B. breve M-16V and L. plantarum NumRes8. Results: Of the panel of 6 strains, B. breve M-16V and L. plantarum NumRes8 inhibited (1) the response to methacholine, (2) reduced the number of eosinophils in the bronchoalveolar lavage fluid, (3) reduced both OVA-specific IgE and (4) OVA-specific IgG1, whereas the other strains did not affect all these parameters simultaneously. B. breve M-16V but not L. plantarum NumRes8 reduced interleukin 4, interleukin 5 and interleukin 10. Furthermore, B. breve M-16V but not L. plantarum NumRes8 reduced acute allergic skin reactions to OVA. Conclusion: B. breve M-16V was identified as the most potent antiallergic strain.

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Section: Discussionmentioning

confidence: 99%

Oral Treatment with Probiotics Reduces Allergic Symptoms in Ovalbumin-Sensitized Mice: A Bacterial Strain Comparative Study

Hougee

Vriesema

Wijering³

et al. 2009

Int Arch Allergy Immunol

Self Cite

154

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“…The effect of PDE‐4 inhibitors has not been assessed in this model, and it was the aim of this study to determine the effects of rolipram, a selective PDE‐4 inhibitor ( Torphy, 1998 ) on the pulmonary eosinophilia and AHR in allergic mice. Experiments were also performed to assess the role of adrenals on the actions of rolipram by studying the effect of adrenalectomy, treatment with metyrapone, a corticosterone synthesis inhibitor ( De Bie et al ., 1996 ), and treatment with propranolol, a β‐adrenoceptor antagonist ( Underwood et al ., 1997 ).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of pulmonary eosinophilia and airway hyperresponsiveness in allergic mice by rolipram: involvement of endogenously released corticosterone and catecholamines

Kung¹,

Crawley²,

Luo³

et al. 2000

British J Pharmacology

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1 This study investigates the role of adrenal-derived catecholamines and corticosterone on the inhibition by rolipram, a phosphodiesterase (PDE)-4 inhibitor, of pulmonary eosinophilia and airway hyperresponsiveness (AHR) in allergic mice. 2 The following experimental groups were studied in mice sensitized and challenged with ovalbumin (OVA): normal, adrenalectomized, propranolol (b-adrenoceptor antagonist) and metyrapone (corticosterone synthesis inhibitor) treated. These interventions were studied both in the absence and in the presence of rolipram. Eosinophil numbers in the bronchoalveolar lavage (BAL) and AHR to methacholine were measured 24 h after OVA challenge. 3 Treatment of sensitized mice with rolipram (0.3 ± 10 mg kg 71 , p.o.), inhibited pulmonary eosinophilia and the AHR to methacholine in OVA-challenged mice. 4 Adrenalectomy increased the number of eosinophils in the BAL of OVA-challenged mice but had no e ect on AHR to methacholine. Adrenalectomy attenuated both the rolipram-induced inhibition of BAL eosinophilia and AHR to methacholine in OVA challenged mice. Propranolol (10 mg kg 71 , p.o.) had no e ect on the inhibition of eosinophilia by rolipram but attenuated the inhibition of AHR to methacholine in OVA challenged mice. On the other hand, metyrapone (10 mg kg 71 , p.o.) attenuated the inhibition of eosinophilia by rolipram but had no e ect on the inhibition of AHR to methacholine in OVA challenged mice. Metyrapone-treatment alone increased the number of eosinophils in the BAL of OVA-challenged mice. 5 These results identify an important role for adrenal-derived catecholamines and corticosterone on the inhibition of pulmonary eosinophilia and AHR by rolipram in allergic mice.

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“…For example, one of the most effective treatments for patients with allergic asthma and particularly for those with chronic disease is glucocorticoids. They have been used in mouse models to test effects on lung inflammation, airway remodeling, AHR, and immunoglobulin production [137, 142, 143, 144, 145, 146]. We chose to test effectiveness of corticosteroids on established experimental allergic asthma in mice [147].…”

Section: What Do the Mouse Models Teach Us About Treating Allergic DImentioning

confidence: 99%

Do Mouse Models of Allergic Asthma Mimic Clinical Disease?

Epstein¹

2004

Int Arch Allergy Immunol

132

108

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Experimental mouse models of allergic asthma established almost 10 years ago offered new opportunities to study disease pathogenesis and to develop new therapeutics. These models focused on the factors governing the allergic immune response, on modeling clinical behavior of allergic asthma, and led to insights into pulmonary pathophysiology. Although mouse models rarely completely reproduce all the features of human disease, after sensitization and respiratory tract challenges with antigen, wild-type mice develop a clinical syndrome that closely resembles allergic asthma, characterized by eosinophilic lung inflammation, airway hyperresponsiveness (AHR), increased IgE, mucus hypersecretion, and eventually, airway remodeling. There are, however, differences between mouse and human physiology that threaten to limit the value of mouse models. Three examples of such differences relate to both clinical manifestations of disease and underlying pathogenesis. First, in contrast to patients who have increased methacholine-induced AHR even when they are symptom-free, mice exhibit only transient methacholine-induced AHR following allergen exposure. Second, chronic allergen exposure in patients leads to chronic allergic asthma, whereas repeated exposures in sensitized mice causes suppression of disease. Third, IgE and mast cells, in humans, mediate early- and late-phase allergic responses, though both are unnecessary for the generation of allergic asthma in mice. Taken together, these observations suggest that mouse models of allergic asthma are not exact replicas of human disease and thus, question the validity of these models. However, observations from mouse models of allergic asthma support many existing paradigms, although some novel discoveries in mice have yet to be verified in patients. This review presents an overview of the clinical aspects of disease in mouse models of allergic asthma emphasizing (1) the factors influencing the pathophysiological responses during the initiation and perpetuation of disease, (2) the utility of mouse models for studying clinical manifestations of disease, and (3) the applicability of mouse models for testing new treatments for allergic asthma.

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Effect of dexamethasone and endogenous corticosterone on airway hyperresponsiveness and eosinophilia in the mouse

Cited by 56 publications

References 28 publications

Oral Treatment with Probiotics Reduces Allergic Symptoms in Ovalbumin-Sensitized Mice: A Bacterial Strain Comparative Study

Oral Treatment with Probiotics Reduces Allergic Symptoms in Ovalbumin-Sensitized Mice: A Bacterial Strain Comparative Study

Inhibition of pulmonary eosinophilia and airway hyperresponsiveness in allergic mice by rolipram: involvement of endogenously released corticosterone and catecholamines

Do Mouse Models of Allergic Asthma Mimic Clinical Disease?

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