Ragweed-specific antibodies in bronchoalveolar lavage fluids and serum before and after segmental lung challenge: IgE and IgA associated with eosinophil degranulation.
BACKGROUND
Migration of eosinophils and release of eosinophil degranulation products into bronchoalveolar lavage fluid is a consistent finding in studies of late responses to allergen challenge in the lung. However, the mechanism of eosinophil activation and release of eosinophil products in vivo is unclear.


OBJECTIVE
We investigated the hypothesis that antigen-specific IgG, IgA, secretory IgA, or IgE is responsible for the eosinophil activation observed in the late-phase pulmonary reaction.


METHODS
Ragweed-specific IgE, IgA, secretory IgA, and IgG were measured by monoclonal antibody-based immunoassays in bronchoalveolar lavage (BAL) fluid and in serum from 19 asthmatic subjects allergic to ragweed and six healthy nonallergic control subjects before and 20 hours after segmental lung challenge with ragweed extract. Eosinophil cationic protein (ECP) was also measured in BAL fluid as a marker of eosinophil activation.


RESULTS
Most allergic asthmatic subjects had detectable levels of ragweed-specific IgE, IgA, and IgG in their serum and BAL fluid, whereas normal subjects had ragweed-specific IgA with no ragweed-specific IgE and little ragweed-specific IgG. IgA was the dominant ragweed-specific antibody isotype in BAL fluids. Ragweed-specific sIgA (r[s] = 0.52, p = 0.02) and IgA (r[s] = 0.50, p = 0.03) in BAL fluid after segmental lung challenge were significantly correlated with ECP. Ragweed-specific IgE and IgA in serum also correlated with ECP (r[s] = 0.74, p < 0.001 and r[s] = 0.48, p = 0.04, respectively).


CONCLUSIONS
The correlation of allergen-specific IgA and IgE antibody levels with ECP as a marker of eosinophil degranulation suggests an important role for IgE antibodies in allergic pulmonary inflammation and a potential role for antigen-specific IgA in eosinophil degranulation in the lung after antigen challenge.
Peebles
R S
RS
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Md., USA.
Liu
M C
MC
Adkinson
N F
NF
Lichtenstein
L M
LM
Hamilton
R G
RG
D000328:Adult; D000918:Antibody Specificity; D001249:Asthma / Q000097:blood / Q000276:immunology* / Q000378:metabolism; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry*; D015550:Cell Degranulation / Q000502:physiology; D004804:Eosinophils / Q000166:cytology / Q000276:immunology*; D000939:Epitopes / Q000032:analysis / Q000097:blood / Q000276:immunology; D005260:Female; D006801:Humans; D007070:Immunoglobulin A / Q000032:analysis* / Q000097:blood / Q000276:immunology; D007071:Immunoglobulin A, Secretory / Q000032:analysis / Q000097:blood / Q000276:immunology; D007073:Immunoglobulin E / Q000032:analysis* / Q000097:blood / Q000276:immunology; D007074:Immunoglobulin G / Q000032:analysis / Q000097:blood / Q000276:immunology; D007132:Immunoglobulin Isotypes / Q000032:analysis / Q000097:blood / Q000276:immunology; D008297:Male
D000939:Epitopes; D007070:Immunoglobulin A; D007071:Immunoglobulin A, Secretory; D007074:Immunoglobulin G; D007132:Immunoglobulin Isotypes; D007073:Immunoglobulin E