Recent studies from our lab proposed that human surfactant proteins A (SP-A) and D (SP-D) strengthen the innate immune response against Aspergillus fumigatus and showed that they inhibit the specific IgE binding and histamine release at their physiological concentrations by interacting with glycosylated allergens and antigens of A.fumigatus.The present study examined the effect of native human pulmonary surfactant protein A (SP-A), surfactant protein D (SP-D)and recombinant surfactant protein D (r SP-D) on various immunological responses to allergens and antigens of A.fumigatus in a murine model of Allergic Bronchopulmonary Aspergillosis (ABPA). In this study physiological concentrations of surfactant proteins were administered intranasally to the mice previously immunised with A.fumigatus antigens and allergens. The effect of surfactant proteins were studied on levels of specific IgG and specific IgE antibodies, peripheral eosinophilia, pulmonary eosinophilia and interleukin profile. The ABPA mice model developed during the study exhibited high levels of specific IgG and specific IgE antibodies, peripheral and pulmonary eosinophils and increased level of Th2 type cytokines (IL-4 and IL-5) in splenic supematants in comparison to control mice.On intranasal administration of physiological concentrations of SP-A. SP-D and r SP-D the elevated levels of specific IgG and specific IgE antibodies, peripheral and pulmonary eosinophil count,IL-4 and IL-5 cytokines were observed to decrease. The IFNgamma levels however showed an increase indicating a shift from predominant Th2 type to the Thl type of immune response.These observations suggest that human surfactant proteins A and D protect the lungs from the immune mediated damage initiated by antigens and allergens of A.fumigatus One mechanism involved in this type of protection includes direct interaction of pulmonary surfactant proteins with glycosylated allergens and antigens.However other mechanisms underlying this protection may involve influence of SP-A and SP-D on pulmonary leucocytes.alveolar macrophages and type 11 cells.
Full conference title:
2000 American Academy of Allergy, Asthma, and Immunology Annual Meeting
- AAAAI 2000 (56th)