Induction of late airway response was involved in serum antigen-specific immunoglobulin G in rats

Miyagawa, Naoki; Iwasaki, Hidenori; Kato, Toshinobu; Tanaka, Masaru; Shibata, Tsutomu; Wakitani, Korekiyo

doi:10.1016/j.intimp.2008.09.003

Cited by 8 publications

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“…8) In addition, repeated antigen inhalation by sensitized rats converts IAR to LAR, a reaction triggered by antigen-specific immunoglobulin G (IgG). 9) In the present study, the pharmacological profiles of rat LAR were examined using rat LAR model. To clarify the pharmacological profile of rat LAR, the effects of antiasthmatic drugs including salbutamol (b 2 -agonist), ketotifen (antihistamine), pranlukast (anti-leukotriene C 4 /D 4 /E 4 ), and prednisolone (steroid) were evaluated.…”

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Pharmacological Analysis of Antigen-Induced Late Airway Response in Rats

Miyagawa

Iwasaki

Kato

et al. 2009

Biological & Pharmaceutical Bulletin

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Bronchial asthma is one of the most common allergic diseases in the world, and is considered a complex inflammatory disorder of the airways with various pathophysiological features.1) The exposure of asthmatics to specific antigens causes airway symptoms which can be generally distinguished into two predominant airway reactions, an immediate airway response (IAR) and a late airway response (LAR). 2,3)The pharmacological profiles of antigen-induced IAR and LAR have been determined using animal models, especially in the guinea pig. For example, it is known that antileukotrienes reduce LAR in guinea pig, while antihistamines do not. 4,5) On the other hand, inhalation of a b 2 -agonist like salbutamol, which directly inhibits the contraction of airway smooth muscle, diminishes IAR but not LAR.6) Further, anti-IL-5 monoclonal antibody decrease infiltration of eosinophils into the tracheal wall, and also markedly suppresses the development of LAR in guinea pig. 7)In recent years, the pharmaceutical targets for new asthmatic drugs have become more immunologically diverse and specific, and detailed immunological analysis of mechanisms in animal models is required to determine with precision the efficacies of new drug candidates. However, the guinea pig model is not sufficient for this purpose, since immunological and genetic research on guinea pigs has not been performed in detail.In this regard, we have examined the pharmacological and immunological characteristics of ovalbumin (OVA)-induced IAR and LAR in the rat. Briefly, rat IAR exhibits diverse immunological characteristics, i.e. a quick phase (3-6 min after challenge) caused by the exocytosis of mediators in CTMCs and an early phase (6-30 min after challenge) mediated by leukotriene (LT) and TXA 2 .8) In addition, repeated antigen inhalation by sensitized rats converts IAR to LAR, a reaction triggered by antigen-specific immunoglobulin G (IgG). 9)In the present study, the pharmacological profiles of rat LAR were examined using rat LAR model. To clarify the pharmacological profile of rat LAR, the effects of antiasthmatic drugs including salbutamol (b 2 -agonist), ketotifen (antihistamine), pranlukast (anti-leukotriene C 4 /D 4 /E 4 ), and prednisolone (steroid) were evaluated. In addition, the involvement of cell infiltration in bronchoalveolar lavage fluid (BALF) and pulmonary edema in LAR were investigated in the rat model. MATERIALS AND METHODS AnimalsMale Sprague-Dawley (SD) rats were purchased from Charles River Japan, Inc. (CRJ, Yokohama, Japan) and individually housed in plastic cages maintained under specific pathogen-free conditions at a room temperature of 23.0Ϯ3.0°C and air humidity of 55Ϯ15% in a 12-h light/dark cycle environment. The rats were given a standard laboratory chow diet (CRF-1, Oriental Yeast, Tokyo, Japan) and water ad libitum. All experiments complied with the Guidelines for Animal Experimentation of our laboratories.Compounds The antihistamine ketotifen (Sigma-Aldrich Co.); anti-LT (leukotriene C 4 /D 4 /E 4 receptor antagonist) pranlukas...

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confidence: 99%

Pharmacological Analysis of Antigen-Induced Late Airway Response in Rats

Miyagawa

Iwasaki

Kato

et al. 2009

Biological & Pharmaceutical Bulletin

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“…Although antigen-specific IgG is induced after antigen inhalation, its role in bronchial asthma remains unknown. OVA-specific IgG in rat-sera, such as IgG1 and IgG2a, is reported to increase on day 21 after OVA inhalation in asthmatic models induced by OVA [8]. Platts-Mills et al demonstrated a progressive increase in specific serum IgG titers with extended exposure and a prevalence of Th2 cytokine-dependent IgG in cats and dogs [9].…”

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Antigen-Specific IgG ameliorates allergic airway inflammation via Fcγ receptor IIB on dendritic cells

et al. 2011

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BackgroundThere have been few reports on the role of Fc receptors (FcRs) and immunoglobulin G (IgG) in asthma. The purpose of this study is to clarify the role of inhibitory FcRs and antigen presenting cells (APCs) in pathogenesis of asthma and to evaluate antigen-transporting and presenting capacity by APCs in the tracheobronchial mucosa.MethodsIn FcγRIIB deficient (KO) and C57BL/6 (WT) mice, the effects of intratracheal instillation of antigen-specific IgG were analysed using the model with sensitization and airborne challenge with ovalbumin (OVA). Thoracic lymph nodes instilled with fluorescein-conjugated OVA were analysed by fluorescence microscopy. Moreover, we analysed the CD11c+ MHC class II+ cells which intaken fluorescein-conjugated OVA in thoracic lymph nodes by flow cytometry. Also, lung-derived CD11c+ APCs were analysed by flow cytometry. Effects of anti-OVA IgG1 on bone marrow dendritic cells (BMDCs) in vitro were also analysed. Moreover, in FcγRIIB KO mice intravenously transplanted dendritic cells (DCs) differentiated from BMDCs of WT mice, the effects of intratracheal instillation of anti-OVA IgG were evaluated by bronchoalveolar lavage (BAL).ResultsIn WT mice, total cells and eosinophils in BAL fluid reduced after instillation with anti-OVA IgG1. Anti-OVA IgG1 suppressed airway inflammation in hyperresponsiveness and histology. In addition, the number of the fluorescein-conjugated OVA in CD11c+ MHC class II+ cells of thoracic lymph nodes with anti-OVA IgG1 instillation decreased compared with PBS. Also, MHC class II expression on lung-derived CD11c+ APCs with anti-OVA IgG1 instillation reduced. Moreover, in vitro, we showed that BMDCs with anti-OVA IgG1 significantly decreased the T cell proliferation. Finally, we demonstrated that the lacking effects of anti-OVA IgG1 on airway inflammation on FcγRIIB KO mice were restored with WT-derived BMDCs transplanted intravenously.ConclusionAntigen-specific IgG ameliorates allergic airway inflammation via FcγRIIB on DCs.

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Molecular Basis for Downregulation of C5a-Mediated Inflammation by IgG1 Immune Complexes in Allergy and Asthma

Pandey

2013

Curr Allergy Asthma Rep

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Allergy and asthma are triggered primarily by the binding of allergen-specific immunoglobulin E (IgE)-allergen complexes to their receptors, recognition of the allergens by antigen-presenting cells, and allergen presentation to the T cells. These events lead to mucus secretions, runny nose, itchy eyes, sneezing, airway hyperresponsiveness, and nasal congestion. Complement 5a (C5a) has emerged as a central molecule that mediates these allergic reactions. Many allergens and allergen-specific IgG immune complexes (IgG-ICs) cause complement activation and C5a generation. C5a interaction with its receptor (C5aR) leads to the infiltration and activation of several immunologic cell types and the secretion of pathogenic inflammatory and proinflammatory mediators. However, IgG1-IC binding to the IgG inhibitory Fc gamma receptor (FcγRIIB) suppresses C5aR-mediated inflammatory signaling and, hence, may reduce the inflammatory immune responses through this FcγRIIB-mediated pathway. Reviews of the IgG1-IC interactions with C5a-mediated inflammatory immune responses suggest that IgG1-IC-C5a inhibitory therapy may reduce inflammation in allergic diseases.

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Induction of late airway response was involved in serum antigen-specific immunoglobulin G in rats

Cited by 8 publications

References 18 publications

Pharmacological Analysis of Antigen-Induced Late Airway Response in Rats

Pharmacological Analysis of Antigen-Induced Late Airway Response in Rats

Antigen-Specific IgG ameliorates allergic airway inflammation via Fcγ receptor IIB on dendritic cells

Molecular Basis for Downregulation of C5a-Mediated Inflammation by IgG1 Immune Complexes in Allergy and Asthma

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