Antigen-specific IgE and IgA antibodies in bronchoalveolar lavage fluid are associated with stronger antigen-induced late phase reactions.
The mechanism(s) leading to the development of late phase allergic reactions is (are) unknown. Previous studies have indicated that a relationship between serum IgE and the late phase exists. To explore the relationships between allergen-specific immunoglobulins in bronchoalveolar lavage (BAL) fluids and the magnitude of airflow limitation during the late phase response to inhaled allergen. Ragweed-specific IgE, IgA, secretory IgA (sIgA) and IgG were measured in BAL fluid and in the serum 1-5 weeks before whole lung antigen challenge with ragweed extract, in 16 ragweed allergic asthmatics. In addition, BAL and serum eosinophil cationic protein (ECP) and BAL fibrinogen levels were determined and BAL cells counted and differentiated. The latter procedures were repeated in a second BAL performed 24 h after the end of the ragweed challenge. After the challenge, lung function was monitored hourly for 8 h, to record the magnitude of airflow limitation. Ragweed-specific immunoglobulins were detected in 25% to 37.5% of BAL samples. Compared to the subjects with undetectable BAL fluid ragweed-specific IgE levels at baseline, those with detectable antibodies had stronger late phase reactions as determined by the nadir of FEV1 between hours 4 and 8 after the ragweed inhalation challenge (P = 0.0007). Allergen-induced changes in BAL ECP and fibrinogen levels were also higher in those subjects with detectable ragweed-specific IgE in baseline fluids (P = 0.03 and P = 0.005, respectively). Significant relationships between BAL antigen-specific IgA, serum ragweed-specific IgE and IgA and the late phase reaction were also found. The results of this study point towards the possibility that allergen-specific IgE and IgA may be independently involved in the pathogenesis of the late phase reaction. This notion merits further exploration.
Peebles
R S
RS
Divisions of Clinical Immunology and Pulmonary and Critical Care Medicine, Johns Hopkins Asthma & Allergy Center, Johns Hopkins University School of Medicine, 5501 Hopkins Bayview Circle, Baltimore, Maryland 21224, USA.
Hamilton
R G
RG
Lichtenstein
L M
LM
Schlosberg
M
M
Liu
M C
MC
Proud
D
D
Togias
A
A
D000328:Adult; D000485:Allergens / Q000276:immunology; D000941:Antigens / Q000276:immunology; D001249:Asthma / Q000276:immunology*; D001798:Blood Proteins / Q000096:biosynthesis; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology*; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000276:immunology; D005260:Female; D005340:Fibrinogen / Q000096:biosynthesis; D005541:Forced Expiratory Volume; D006801:Humans; D007070:Immunoglobulin A / Q000096:biosynthesis*; D007073:Immunoglobulin E / Q000096:biosynthesis*; D007958:Leukocyte Count; D008297:Male; D010936:Plant Extracts / Q000276:immunology; D011058:Pollen / Q000276:immunology*; D012260:Ribonucleases
D000485:Allergens; D000941:Antigens; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D007070:Immunoglobulin A; D010936:Plant Extracts; D007073:Immunoglobulin E; D005340:Fibrinogen; D012260:Ribonucleases