120. The influence of genetic factors and antigen dose on IgE production in rats

Pauwels, Romain; Bazin, Hervé; Platteau, Bernadette; Straeten, M. Van Der

doi:10.1016/0091-6749(78)90359-7

Cited by 20 publications

(28 citation statements)

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“…The threshold dose of OA, 0.1-1 ¡ig, for a primary tissue response to be induced in SD rats with Al(OHfi is very similar to that reported for induction of OAIgE-antibody responses in many rat strains [2,13,[25][26][27], Although SD rats are generally not considered as high OA-IgE-antibody producers [2,26,32], but com pare [28], they turned out to be good responders in the present system provided that suitable adjuvant condi tions were chosen. Consistent lung tissue, tracheal, and serosal mast cell responses in general seemed to be induced at the same immunization dose of OA, but unexpectedly the temporal pattern of development and the magnitude of the responses tended to disso ciate under various conditions.…”

Section: Discussionmentioning

confidence: 54%

Antigen-Induced Release of Histamine from Rat Tissues in vitro: Dissociation in Development of Serosal Mast Cell, Lung Tissue, and Tracheal Tissue Response Capacity

Bergstrand¹,

Frick²,

Lindhqvist³

et al. 1982

Int Arch Allergy Immunol

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We examined the temporal development and the fading in Sprague Dawley rats, actively sensitized to ovalbumin (OA), of the capacity of serosal mast cells, chopped lung tissue, and occasionally chopped tracheal tissue, to respond at antigen challenge in vitro with histamine release. Response capacity of both serosal mast cells and lung tissue developed within 2–3 weeks after injection of 1 μg OA or more together with 100 mg of alum. Maximum response capacity was observed in cells and tissue from animals injected with 10 μg OA, part of the response capacity then remained until 3 months after immunization. Development of serosal mast cell reactivity was occasionally dissociated from that of lung tissue. When low amounts of alum (1 or 10 mg) were employed as adjuvant, lung tissue reactivity could be induced in the virtual absence of serosal mast cell response capacity. Silica gel was less efficient than alum as an adjuvant for induction of a primary response, but ‘secondary’ tissue responses could be induced when silica gel was used as an adjuvant. Pretreatment of the animals with cyclophosphamide before the booster injection enhanced and prolonged the response capacity of lung tissue. Animals injected with OA together with Freund’s complete adjuvant did not provide responding serosal mast cells; response capacity of lung tissue varied with immunization dose of antigen. Antigen-induced histamine release from chopped tracheal tissue did not correlate to response capacity of lung tissue. Thus, the development in the rat of response capacity with respect to antigen-induced histamine release dissociates for serosal mast cells, lung tissue, and tracheal tissue.

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Section: Discussionmentioning

confidence: 54%

Antigen-Induced Release of Histamine from Rat Tissues in vitro: Dissociation in Development of Serosal Mast Cell, Lung Tissue, and Tracheal Tissue Response Capacity

Bergstrand¹,

Frick²,

Lindhqvist³

et al. 1982

Int Arch Allergy Immunol

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“…It is difficult to know the exact reasons for the difference, but this highlights the usefulness of examining different systems before making firm conclusions about immunoregulatory mechanisms. One difference may be that our experiments were performed in the Brown Norway rat, which seems to favor Th2 responses and thus has been used successfully in a variety of other Th2 systems (22)(23)(24). Many features of Th2 asthma occur in this rat model (4 -6, 25), including adoptive transfer of BHR and airway eosinophilia by CD4 ϩ T cells (4,6,7) and by allergen-specific Th2 lines, as shown in this study.…”

Section: Discussionmentioning

confidence: 99%

“…The Brown Norway rat is a useful model for studying Th2 responses such as helminthic parasite infestations (22), IgE production (23), drug allergies (24), and asthma. Sensitization with OVA followed by OVA airway challenge leads to eosinophilic airway inflammation, local infiltration of activated Th2 cells, and BHR (4,5,25).…”

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confidence: 99%

Allergen-Specific Th1 Cells Counteract Efferent Th2 Cell-Dependent Bronchial Hyperresponsiveness and Eosinophilic Inflammation Partly Via IFN-γ

Huang

MacAry

Eynott

et al. 2001

The Journal of Immunology

122

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Th2 T cell immune-driven inflammation plays an important role in allergic asthma. We studied the effect of counterbalancing Th1 T cells in an asthma model in Brown Norway rats that favors Th2 responses. Rats received i.v. transfers of syngeneic allergen-specific Th1 or Th2 cells, 24 h before aerosol exposure to allergen, and were studied 18–24 h later. Adoptive transfer of OVA-specific Th2 cells, but not Th1 cells, and OVA, but not BSA exposure, induced bronchial hyperresponsiveness (BHR) to acetylcholine and eosinophilia in a cell number-dependent manner. Importantly, cotransfer of OVA-specific Th1 cells dose-dependently reversed BHR and bronchoalveolar lavage (BAL) eosinophilia, but not mucosal eosinophilia. OVA-specific Th1 cells transferred alone induced mucosal eosinophilia, but neither BHR nor BAL eosinophilia. Th1 suppression of BHR and BAL eosinophilia was allergen specific, since cotransfer of BSA-specific Th1 cells with the OVA-specific Th2 cells was not inhibitory when OVA aerosol alone was used, but was suppressive with OVA and BSA challenge. Furthermore, recipients of Th1 cells alone had increased gene expression for IFN-γ in the lungs, while those receiving Th2 cells alone showed increased IL-4 mRNA. Importantly, induction of these Th2 cytokines was inhibited in recipients of combined Th1 and Th2 cells. Anti-IFN-γ treatment attenuated the down-regulatory effect of Th1 cells. Allergen-specific Th1 cells down-regulate efferent Th2 cytokine-dependent BHR and BAL eosinophilia in an asthma model via mechanisms that depend on IFN-γ. Therapy designed to control the efferent phase of established asthma by augmenting down-regulatory Th1 counterbalancing mechanisms should be effective.

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“…Recently many researchers have reported that BN rats are high responders to IgE antibody production [22][23][24] and suitable animals for investigating the mechanism Effect of HSR-609 on Late Phase Nasal Eosinophilia of airway hyperresponsiveness [25][26][27][28][29][30][31]. Moreover, the symptoms of experimental asthma in BN rats are similar to human bronchial asthma in terms of the appearance of IPR and LPR and airway hyperresponsiveness with an accumulation of inflammatory cells in the airways after exposure to antigen [25][26][27][28][29][30][31].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, some investigators have reported that chemotactic factors such as platelet-activating factor, leukotriene B 4 and interleukin-5 (IL-5) may play an important role in the infiltration of eosinophils [16][17][18][19][20][21]. In the present study, we investigated an allergic late phase eosinophilia model in BN rats that were high responders to IgE antibody production [22][23][24] and were observed not only for IPR and LPR but also airway hyperresponsiveness with accumulation of proinflammatory cells after antigen exposure [25][26][27][28][29][30][31].…”

Section: Introductionmentioning

confidence: 99%

Effects of an Amphoteric Antiallergic Agent, HSR-609, on Antigen-Induced Late Phase Nasal Eosinophilia in Brown Norway Rats

Musoh¹,

Nakamura²,

Nagai³

2000

Pharmacology

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The effect of a newly synthesized compound, HSR-609, on rat experimental rhinitis was investigated. In the first part of the study, a new experimental nasal allergic late phase eosinophilia model in Brown Norway (BN) rats was investigated. The increase in the number of antigen inhalations resulted in the proportional increase in the number of inflammatory cells such as macrophages, eosinophils and neutrophils in the nasal cavity lavage fluid (NCLF) at 5 h after each inhalation. The number of inflammatory cells reached a maximum 8 h after the antigen perfusion. Submaximum response was observed at 5 h after the antigen provocation. In this system, the serum IgG and IgE antibody titers measured by homologous passive cutaneous anaphylaxis were 160 and 640, respectively. In the second part of the study, the effects of prednisolone, cetirizine and a newly synthesized amphoteric antiallergic agent, HSR-609, on this allergic late nasal eosinophilia and neutrophilia in BN rats were investigated. Prednisolone and HSR-609 significantly inhibited the increase in the number of eosinophils in the NCLF but not cetirizine. Furthermore, prednisolone showed the inhibition of the increase in the number of macrophages and neutrophils in NCLF. These results suggest that this late phase eosinophilia model in the nose of BN rats may be useful for investigating the therapeutic drugs for nasal allergy and a newly synthesized amphoteric antiallergic agent, HSR-609, may be useful for the treatment of allergic rhinitis with eosinophilia.

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120. The influence of genetic factors and antigen dose on IgE production in rats

Cited by 20 publications

References 0 publications

Antigen-Induced Release of Histamine from Rat Tissues in vitro: Dissociation in Development of Serosal Mast Cell, Lung Tissue, and Tracheal Tissue Response Capacity

Antigen-Induced Release of Histamine from Rat Tissues in vitro: Dissociation in Development of Serosal Mast Cell, Lung Tissue, and Tracheal Tissue Response Capacity

Allergen-Specific Th1 Cells Counteract Efferent Th2 Cell-Dependent Bronchial Hyperresponsiveness and Eosinophilic Inflammation Partly Via IFN-γ

Effects of an Amphoteric Antiallergic Agent, HSR-609, on Antigen-Induced Late Phase Nasal Eosinophilia in Brown Norway Rats

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