Pseudomonas respiratory infection in cystic fibrosis

A possible defect in opsonic IgG antibody?

R. B. Fick, H. Y. Reynolds

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Chronic Pseudomonas aeruginosa infections of the respiratory tract of people with cystic fibrosis (CF) usually are impossible to eradicate and greatly influence their health and longevity. General mechanisms of host defense are not impaired in this disease, except that serum does not support optimal phagocytosis of pseudomonas bacteria by alveolar macrophages and lung ciliary clearance is diminished, perhaps because of the accumulation of tenacious, purulent secretions in bronchiectatic airways and not by a defect in cilia structure or inhibitors of ciliary function. To investigate the defect in phagocytosis, we postulated that opsonic antibody might not be functioning well. Samples of purified IgG antibody against the typical strain of mucoid pseudomonas were prepared on immunoadsorbents, using CF sera and normal sera from volunteers previously immunized with a pseudomonas vaccine. CF IgG opsonin was found to agglutinate and coat well pseudomonas, but not to adhere or attach well to the surface of human alveolar macrophages, hence a defect in the function of the Fc portion of IgG was noted. In extending this analysis to CF lung secretions obtained by broncho-alveolar lavage, IgG antibody was purified exactly as from serum. Although this IgG had good agglutinating activity, much of it was fragmented (5 S size) and found to lack its Fc portion. It was evident that proteolytic enzymes in the purulent lavage secretions could cleave IgG. This activity was localized to a metallo-proteinase elaborated by the mucoid strain of pseudomonas. Thus, CF IgG may have reduced opsonic antibody function because of a molecular change in the Fc portion; this defect is magnified in the infected CF lung where a bacterial protease can actually fragment IgG and further impair its opsonic activity which is already marginal.

Original languageEnglish (US)
Pages (from-to)151-161
Number of pages11
JournalClinical Respiratory Physiology
Volume19
Issue number2
StatePublished - 1983

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Pseudomonas Infections
Cystic Fibrosis
Respiratory Tract Infections
Immunoglobulin G
Antibodies
Pseudomonas
Peptide Hydrolases
Therapeutic Irrigation
Alveolar Macrophages
Serum
Phagocytosis
Lung
Pseudomonas Vaccines
Opsonin Proteins
Immunosorbents
Cilia
Respiratory System
Pseudomonas aeruginosa
Healthy Volunteers
Bacteria

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine

Cite this

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title = "Pseudomonas respiratory infection in cystic fibrosis: A possible defect in opsonic IgG antibody?",
abstract = "Chronic Pseudomonas aeruginosa infections of the respiratory tract of people with cystic fibrosis (CF) usually are impossible to eradicate and greatly influence their health and longevity. General mechanisms of host defense are not impaired in this disease, except that serum does not support optimal phagocytosis of pseudomonas bacteria by alveolar macrophages and lung ciliary clearance is diminished, perhaps because of the accumulation of tenacious, purulent secretions in bronchiectatic airways and not by a defect in cilia structure or inhibitors of ciliary function. To investigate the defect in phagocytosis, we postulated that opsonic antibody might not be functioning well. Samples of purified IgG antibody against the typical strain of mucoid pseudomonas were prepared on immunoadsorbents, using CF sera and normal sera from volunteers previously immunized with a pseudomonas vaccine. CF IgG opsonin was found to agglutinate and coat well pseudomonas, but not to adhere or attach well to the surface of human alveolar macrophages, hence a defect in the function of the Fc portion of IgG was noted. In extending this analysis to CF lung secretions obtained by broncho-alveolar lavage, IgG antibody was purified exactly as from serum. Although this IgG had good agglutinating activity, much of it was fragmented (5 S size) and found to lack its Fc portion. It was evident that proteolytic enzymes in the purulent lavage secretions could cleave IgG. This activity was localized to a metallo-proteinase elaborated by the mucoid strain of pseudomonas. Thus, CF IgG may have reduced opsonic antibody function because of a molecular change in the Fc portion; this defect is magnified in the infected CF lung where a bacterial protease can actually fragment IgG and further impair its opsonic activity which is already marginal.",
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Pseudomonas respiratory infection in cystic fibrosis : A possible defect in opsonic IgG antibody? / Fick, R. B.; Reynolds, H. Y.

In: Clinical Respiratory Physiology, Vol. 19, No. 2, 1983, p. 151-161.

Research output: Contribution to journalArticle

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AU - Reynolds, H. Y.

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AB - Chronic Pseudomonas aeruginosa infections of the respiratory tract of people with cystic fibrosis (CF) usually are impossible to eradicate and greatly influence their health and longevity. General mechanisms of host defense are not impaired in this disease, except that serum does not support optimal phagocytosis of pseudomonas bacteria by alveolar macrophages and lung ciliary clearance is diminished, perhaps because of the accumulation of tenacious, purulent secretions in bronchiectatic airways and not by a defect in cilia structure or inhibitors of ciliary function. To investigate the defect in phagocytosis, we postulated that opsonic antibody might not be functioning well. Samples of purified IgG antibody against the typical strain of mucoid pseudomonas were prepared on immunoadsorbents, using CF sera and normal sera from volunteers previously immunized with a pseudomonas vaccine. CF IgG opsonin was found to agglutinate and coat well pseudomonas, but not to adhere or attach well to the surface of human alveolar macrophages, hence a defect in the function of the Fc portion of IgG was noted. In extending this analysis to CF lung secretions obtained by broncho-alveolar lavage, IgG antibody was purified exactly as from serum. Although this IgG had good agglutinating activity, much of it was fragmented (5 S size) and found to lack its Fc portion. It was evident that proteolytic enzymes in the purulent lavage secretions could cleave IgG. This activity was localized to a metallo-proteinase elaborated by the mucoid strain of pseudomonas. Thus, CF IgG may have reduced opsonic antibody function because of a molecular change in the Fc portion; this defect is magnified in the infected CF lung where a bacterial protease can actually fragment IgG and further impair its opsonic activity which is already marginal.

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