Surfactant proteins A and D protect mice against pulmonary hypersensitivity induced by Aspergillus fumigatus antigens and allergens

Allergic bronchopulmonary aspergillosis (ABPA) is an allergic disorder caused by an opportunistic fungal pathogen, Aspergillus fumigatus (AFU:). Lung surfactant proteins SP-A and SP-D can interact with the glycosylated antigens and allergens of AFU:, inhibit specific IgE binding to these allergens,...

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Bibliographic Details
Published in:The Journal of clinical investigation 2001-02, Vol.107 (4), p.467-475
Main Authors: Madan, T, Kishore, U, Singh, M, Strong, P, Clark, H, Hussain, E M, Reid, K B, Sarma, P U
Format: Article
Language:English
Subjects:
Allergens - immunology
Animals
Antigens, Fungal - immunology
Aspergillus fumigatus
Aspergillus fumigatus - immunology
Cytokines - biosynthesis
Eosinophil Peroxidase
Eosinophilia - etiology
Glycoproteins - pharmacology
Humans
Immunoglobulin E - blood
Immunoglobulin G - blood
Lung - immunology
Lung - pathology
Mice
Mice, Inbred BALB C
Peroxidases - metabolism
Proteolipids - pharmacology
Pulmonary Surfactant-Associated Protein A
Pulmonary Surfactant-Associated Protein D
Pulmonary Surfactant-Associated Proteins
Pulmonary Surfactants - pharmacology
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Summary:Allergic bronchopulmonary aspergillosis (ABPA) is an allergic disorder caused by an opportunistic fungal pathogen, Aspergillus fumigatus (AFU:). Lung surfactant proteins SP-A and SP-D can interact with the glycosylated antigens and allergens of AFU:, inhibit specific IgE binding to these allergens, and block histamine release from sensitized basophils. We have now examined the therapeutic effect of exogenous administration of human SP-A, SP-D, and a recombinant fragment of SP-D (rSP-D), in a murine model of pulmonary hypersensitivity induced by AFU: antigens and allergens, which resembles human ABPA immunologically. The ABPA mice exhibited high levels of AFU:-specific IgG and IgE, blood eosinophilia, extensive infiltration of lymphocytes and eosinophils in the lung sections, and a Th2 cytokine response. Treatment with SP-A, SP-D, and rSP-D lowered blood eosinophilia, pulmonary infiltration, and specific Ab levels considerably, which persisted up to 4 days in the SP-A-treated ABPA mice, and up to 16 days in the SP-D- or rSP-D-treated ABPA mice. The levels of IL-2, IL-4, and IL-5 were decreased, while the level of IFN-gamma was raised in the splenic supernatants of the treated mice, indicating a marked shift from Th2 to Th1 response. These results clearly implicate pulmonary SP-A and SP-D in the modulation of allergic reactions.
ISSN:0021-9738
DOI:10.1172/jci10124