Experimental Pulmonary Eosinophilia in Mice by<i>Ascaris suum</i>Extract

Nogami, Makoto; Suko, Matsunobu; Okudaira, Hirokazu; Miyamoto, Terumasa; Shiga, Junji; Ito, Mamoru; Kasuya, Shiro

doi:10.1164/ajrccm/141.5_pt_1.1289

Cited by 50 publications

(35 citation statements)

References 8 publications

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“…CsA, paradoxically, increased the A. fumigatus-induced lung disease. This latter fmding contrasts with the results of Nogami et ai, who found that CsA efficiently blocked Ascaris antigen-induced pulmonary eosinophilia [35]. However, other reports showed that CsA caused an augmentation of DTH in rats or guinea pigs [36].…”

Section: Discussionmentioning

confidence: 58%

Cyclosporin A increases the pulmonary eosinophilia induced by inhaledAspergillusantigen in mice

Wang¹,

Michel

Fournier

et al. 1993

Clinical and Experimental Immunology

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SUMMARYWe evaluated the effects of anti-inflammatory drugs in a murine model of allergic bronchopulmonary aspergillosis(ABPA). Mice instilled with 100 iigof Aspergi/lu.v fumigatu.s antigen (intranasally, 3 days a week for 3 weeks) developed pulmonary lesions, characterized by a perivascular and pcribronchial eosinophil infiltration, a bronchoaiveoiar Iavage (BAL) eosinophilia, and elevated levels of tolal IgE, total igGI and A. fumigatus-spccific IgGl, Under the same conditions, groups of mice receiving a daily dose of 2 mg/kg dexamcthasone showed decreased numbers oi' eosinophils and lolal cells in BAL, had less numerous eosinophils in their pulmonary infiltrates, and had lower levels ofserum and BAL fluid total IgE, total IgGl and A. fumigatu.s-spec\fic IgGl. Conversely, groups of mice pretreated with an immunosuppressive agent, cyclosporin A (CsA)at adoseof 5()mg/kg, three times per week, developed pulmonary lesions with enhanced lung cosinophilic influx and increased total IgE levels, both in serum and in BAL lluid. These findings show thai dexamelhasone polenlly prevents the murine immunopathologic response to A. fumigatus. The eflect of CsA on this inflammatory response was paradoxical, insofar as it suggests an activation ofthe T helper 2 subset, which Lip-rcguiales cosinophii recruitment and IgK production.Keywords Aspergitlus fumigaius pulmonary eosinophilia dexamcthasonc cyclosporin A total and specific hypergammaglobuUnaemia ABPA

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Section: Discussionmentioning

confidence: 58%

Cyclosporin A increases the pulmonary eosinophilia induced by inhaledAspergillusantigen in mice

Wang¹,

Michel

Fournier

et al. 1993

Clinical and Experimental Immunology

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“…Using these mice, a series of studies showed that MCs play an important role in the airway response (30,(33)(34)(35)(36). Although some studies showed that MC deficiency resulted in attenuated eosinophil-mediated airway inflammation (34,37), other studies indicated a lack of MC participation in AHR (38)(39)(40). These conflicting roles for MCs may be due to experimental variables, such as the inclusion or omission of artificial adjuvants, or the use of relatively low doses of Ag for sensitization (30,33,34,36).…”

Section: Discussionmentioning

confidence: 99%

Role of Mast Cells and Basophils in IgE Responses and in Allergic Airway Hyperresponsiveness

Sawaguchi

Tanaka

Nakatani

et al. 2012

The Journal of Immunology

147

153

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We established a diphtheria toxin (DT)-based conditional deletion system using Il4 enhancer elements previously shown to be specific for IL-4 production in mast cells (MCs) or basophils (Mas-TRECK and Bas-TRECK mice). DT treatment of Bas-TRECK mice resulted in specific deletion of basophils, whereas both MCs and basophils were deleted in Mas-TRECK mice. DT-treated Mas-TRECK mice had impaired passive cutaneous anaphylaxis, IgE-mediated passive systemic anaphylaxis, and IgE-mediated chronic allergic inflammation, whereas DT-treated Bas-TRECK mice had impaired IgE-mediated chronic allergic inflammation. Using these mice, we also sought to tease out the role of MCs and basophils in airway hyperresponsiveness (AHR). Although MC deletion resulted in a slight increase in basal Ag-specific IgE levels and significant increases in basal IgE levels, we found that this deletion markedly impaired the AHR effector phase and was accompanied by decreased histamine levels. By contrast, basophil deletion had no effect on the AHR effector phase or on IgE production induced by systemic OVA immunization. Our results, using these newly established Mas-TRECK and Bas-TRECK models, demonstrated an indispensable role for MCs as effector cells in AHR.

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“…When studying mechanisms of allergic airway disease in animal models, mast cell-deficient mice have variable decreases in eosinophil numbers (31,32) following allergen challenge, but systemically sensitized and challenged mast cell-deficient mice are capable of developing a Th2 response, airway inflammation, and AHR similar to WT control mice (33)(34)(35)(36). In most of these studies, allergen sensitization was achieved by systemically injecting the allergen in combination with an adjuvant, while other studies, using less potent sensitization protocols, demonstrated a more obvious role for mast cells in the development of AHR (37,38).…”

Section: Discussionmentioning

confidence: 99%

The Leukotriene B4 Receptor (BLT1) Is Required for Effector CD8+ T Cell-Mediated, Mast Cell-Dependent Airway Hyperresponsiveness

Taube

Miyahara

Ott

et al. 2006

The Journal of Immunology

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Studies in both humans and rodents have suggested that CD8+ T cells contribute to the development of airway hyperresponsiveness (AHR) and that leukotriene B4 (LTB4) is involved in the chemotaxis of effector CD8+ T cells (TEFF) to the lung by virtue of their expression of BLT1, the receptor for LTB4. In the present study, we used a mast cell-CD8-dependent model of AHR to further define the role of BLT1 in CD8+ T cell-mediated AHR. C57BL/6+/+ and CD8-deficient (CD8−/−) mice were passively sensitized with anti-OVA IgE and exposed to OVA via the airways. Following passive sensitization and allergen exposure, C57BL/6+/+ mice developed altered airway function, whereas passively sensitized and allergen-exposed CD8−/− mice failed to do so. CD8−/− mice reconstituted with CD8+ TEFF developed AHR in response to challenge. In contrast, CD8−/− mice reconstituted with BLT1-deficient effector CD8+ T cells did not develop AHR. The induction of increased airway responsiveness following transfer of CD8+ TEFF or in wild-type mice could be blocked by administration of an LTB4 receptor antagonist confirming the role of BLT1 in CD8+ T cell-mediated AHR. Together, these data define the important role for mast cells and the LTB4-BLT1 pathway in the development of CD8+ T cell-mediated allergic responses in the lung.

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Experimental Pulmonary Eosinophilia in Mice byAscaris suumExtract

Cited by 50 publications

References 8 publications

Cyclosporin A increases the pulmonary eosinophilia induced by inhaledAspergillusantigen in mice

Cyclosporin A increases the pulmonary eosinophilia induced by inhaledAspergillusantigen in mice

Role of Mast Cells and Basophils in IgE Responses and in Allergic Airway Hyperresponsiveness

The Leukotriene B4 Receptor (BLT1) Is Required for Effector CD8+ T Cell-Mediated, Mast Cell-Dependent Airway Hyperresponsiveness

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