title: Role of particulate antigens of Aspergillus in murine eosinophilia.
abstract: OBJECTIVE
  Allergic bronchopulmonary aspergillosis, a disabling hypersensitivity lung disease, results from inhalation of Aspergillus fumigatus antigens present in contaminated environments. A murine model has been developed to understand the immune mechanism involved in allergic bronchopulmonary aspergillosis. We have investigated the immunoregulatory role of different physical forms of A.fumigatus antigens, such as A.fumigatus spores, soluble antigens. and soluble antigen coupled inert particles, in the model.
  
  
  METHODS
  BALB/c mice were exposed to soluble A.fumigatus antigens, spores, or inert particles of comparable size to the spores coupled with A.fumigatus soluble antigens. Antibody and eosinophil response, pulmonary pathology, and cytokine expressions were studied.
  
  
  RESULTS
  Peripheral blood eosinophilia and pulmonary inflammation with influx of eosinophils into the lung was detected more in animals exposed to particulate antigens than in those exposed to soluble antigen. However, the total serum IgE and Aspergillus-specific IgG levels showed only a slight increase in the former groups as opposed to elevated levels in animals exposed to soluble antigen. The cytokine expression in in vitro antigen stimulated spleen cells showed a typical Th2 pattern in all antigen-exposed animals. IL-5 mRNA could be detected in the spleen cells cultured with antigen from all groups of antigen-exposed animals.
  
  
  CONCLUSIONS
  Particulate A.fumigatus antigens induced eosinophilia in mice prior to the elevation of serum IgE levels. This pattern of IgE and eosinophilia is reversed with the soluble antigen exposure in this model.
authors.affiliation: Department of Medicine, Medical College of Wisconsin, Milwaukee, USA.
authors.forename: V P
authors.initials: VP
authors.lastname: Kurup
authors.forename: H
authors.initials: H
authors.lastname: Choi
authors.forename: P S
authors.initials: PS
authors.lastname: Murali
authors.forename: A
authors.initials: A
authors.lastname: Resnick
authors.forename: J N
authors.initials: JN
authors.lastname: Fink
authors.forename: R L
authors.initials: RL
authors.lastname: Coffman
mesh_terms: D000818:Animals; D000908:Antibodies, Fungal / Q000276:immunology; D000918:Antibody Specificity; D000946:Antigens, Fungal / Q000502:physiology*; D001229:Aspergillosis, Allergic Bronchopulmonary / Q000150:complications; D001232:Aspergillus fumigatus / Q000276:immunology; D001853:Bone Marrow / Q000201:enzymology; D001854:Bone Marrow Cells; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004802:Eosinophilia / Q000150:complications / Q000276:immunology*; D004804:Eosinophils / Q000201:enzymology; D005260:Female; D007073:Immunoglobulin E / Q000096:biosynthesis; D007371:Interferon-gamma / Q000502:physiology; D015847:Interleukin-4 / Q000502:physiology; D015848:Interleukin-5 / Q000502:physiology; D008168:Lung / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D009195:Peroxidase / Q000032:analysis; D012333:RNA, Messenger / Q000378:metabolism; D013154:Spleen / Q000166:cytology; D013172:Spores, Fungal / Q000276:immunology
chemical_list: D000908:Antibodies, Fungal; D000946:Antigens, Fungal; D016207:Cytokines; D015848:Interleukin-5; D012333:RNA, Messenger; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma; D009195:Peroxidase