Role of IgE in the development of allergic airway inflammation and airway hyperresponsiveness – a murine model

Hamelmann, Eckard; Tadeda, K; Oshiba, Akihiro; Gelfand, EW

doi:10.1034/j.1398-9995.1999.00085.x

Cited by 183 publications

(147 citation statements)

References 49 publications

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“…Production of antigen-specific IgE in response to allergen provocation is a fundamental hallmark of atopic diseases (Burrows et al, 1989;Hamelmann et al, 1999). The crosslinking of antigen to IgE on the surface of mast cells is believed to provide the stimulus for mast cell degranulation in early-phase allergic reactions, an event that precipitates a cascade of inflammatory events in response to allergen (Martin et al, 1989(Martin et al, , 1993Oshiba et al, 1996).…”

Section: Platelet Involvement In Antigen Recognitionmentioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

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Section: Platelet Involvement In Antigen Recognitionmentioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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“…The development of airway inflammation, airway hyperresponsiveness (AHR), mucus production and high serum IgE levels is characteristic of experimental models of asthma [15,16]. CD4+ type 2 helper (Th2) cells play an important role in the production of IgE and the growth and differentiation of mast cells, basophils, and eosinophils [17,18].…”

Section: Introductionmentioning

confidence: 99%

Vitamin D receptor expression by the lung micro-environment is required for maximal induction of lung inflammation

Wittke¹,

Chang²,

Froicu³

et al. 2007

Archives of Biochemistry and Biophysics

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Mice lacking the vitamin D receptor (VDR) are resistant to airway inflammation. Pathogenic immune cells capable of transferring experimental airway inflammation to wildtype (WT) mice are present and primed in the VDR KO mice. Furthermore, the VDR KO immune cells homed to the WT lung in sufficient numbers to induce symptoms of asthma. Conversely, WT splenocytes, Th2 cells and hematopoetic cells induced some symptoms of experimental asthma when transferred to VDR KO mice, but the severity was less than that seen in the WT controls. Interestingly, experimentally induced vitamin D deficiency failed to mirror the VDR KO phenotype suggesting there might be a difference between absence of the ligand and VDR deficiency. Lipopolysaccharide (LPS) induced

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“…The existing literature suggests that a role for IgE or other classes of Abs in murine models of asthma is dependent on experimental variables. As an example, it has been proposed that IgE plays an important role in the development of airway inflammation and AHR only under experimental conditions in which eosinophilic inflammation is relatively low (25).…”

mentioning

confidence: 99%

IgE-Dependent Mast Cell Activation Potentiates Airway Responses in Murine Asthma Models

Mayr

Zuberi

Zhang

et al. 2002

The Journal of Immunology

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We have studied murine models of asthma using FcεRIα-chain-deficient (FcεRIα−/−) mice to investigate the role of IgE-dependent mast cell activation in these models. When mice were either 1) immunized once with OVA in alum i.p. and then challenged with OVA intranasally, or 2) repeatedly immunized with OVA in the absence of adjuvant and subsequently challenged with nebulized OVA, FcεRα−/− mice had significantly fewer eosinophils and lower IL-4 levels in their bronchoalveolar lavage fluid compared with wild-type mice. When mice were given anti-IL-5 antibody before OVA challenge in protocol 1, eosinophilic infiltration into the airways was significantly suppressed in both genotypes, but only FcεRIα−/− mice showed significantly reduced airway hyperresponsiveness (AHR). In addition, when mice immunized and challenged with OVA also received a late OVA provocation at a higher concentration and were then exposed to methacholine, only wild-type mice developed a substantial increase in AHR. Since FcεRI is expressed mainly on mast cells in mouse airways, we conclude that IgE-dependent activation of this cell type plays an important role in the development of allergic airway inflammation and AHR in mice. The models used may be of value for testing inhibitors of IgE or mast cells for development of therapeutic agents for human asthma.

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Role of IgE in the development of allergic airway inflammation and airway hyperresponsiveness – a murine model

Abstract: Role of IgE in the development of allergic airway in¯ammation and airway hyperresponsiveness ± a murine model.Allergy 1999, 54, 297±305.

Cited by 183 publications

References 49 publications

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Vitamin D receptor expression by the lung micro-environment is required for maximal induction of lung inflammation

IgE-Dependent Mast Cell Activation Potentiates Airway Responses in Murine Asthma Models

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