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Longitudinal serum IgG response to Pseudomonas cepacia surface antigens in cystic fibrosis
Author(s) -
Aronoff Stephen C.,
Quinn Francis J.,
Stern Robert C.
Publication year - 1991
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.1950110404
Subject(s) - cystic fibrosis , antibody , pseudomonas aeruginosa , microbiology and biotechnology , bacterial outer membrane , colonization , antigen , titer , immunoglobulin g , antibody titer , medicine , biology , immunology , bacteria , escherichia coli , biochemistry , gene , genetics
In cystic fibrosis (CF), serum antibody against surface antigens of Pseudomonas aeruginosa is detected only after colonization. Since pulmonary acquisition of P. cepacia usually follows colonization with P. aeruginosa and since P. aeruginosa ‐colonized patients with CF have demonstrable antibody against outer membrane proteins of P. cepacia , it appears that acquisition of the latter organism occurs in the presence of specific serum antibody. To test this hypothesis, serum obtained from six P. aeruginosa ‐colonized patients 4 and 2 years prior to and 3 months and 2 years after P. cepacia colonization were assayed for total and specific IgG to P. cepacia outer membrane components. Four patients demonstrated 6‐fold or greater increases in specific IgG titers to whole outer membranes following colonization. By immunoblot, all patients had demonstrable serum IgG against the 27‐ and 36‐kDa outer membrane proteins of P. cepacia 4 and 2 years prior to colonization. Immunoblots after P. cepacia acquisition demonstrated an intensification of the 28‐ and 36‐kDa bands and the appearance of antibody to a very low molecular weight compound which was not hydrolyzed by proteinase K and was present in purified LPS. These observations suggest that low serum titers of antibody against two P. cepacia outer membrane proteins are present in patients with CF prior to P. cepacia colonization, and that these antibodies fail to protect for intrinsic or extrinsic reasons.