Two Distinct Receptors Mediate Nonopsonic Phagocytosis of Different Strains ofPseudomonas aeruginosa
Author(s) -
JohnPaul Heale,
Andrew J. Pollard,
Richard W. Stokes,
David Simpson,
Angela Tsang,
Bonnie G. Massing,
David P. Speert
Publication year - 2001
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/319685
Subject(s) - phagocytosis , opsonin , microbiology and biotechnology , pseudomonas aeruginosa , receptor , phagocyte , biology , antibody opsonization , cd14 , ingestion , macrophage , complement receptor , monoclonal antibody , antibody , bacteria , immunology , complement system , in vitro , biochemistry , genetics
Complement receptor 3 (CR3) mediates both opsonic and nonopsonic phagocytosis of bacteria. Leukocyte adhesion deficiency (LAD) allows for the study of CR3-dependent phagocyte-bacterial ingestion, since LAD phagocytes do not express this receptor. Phagocytes from an infant with LAD were unable to ingest 50% of the Pseudomonas aeruginosa strains studied, which indicates a requirement for CR3. However, the remaining strains were phagocytosed in the absence of CR3, and ingestion was blocked by monoclonal antibodies directed at CD14. This CR3/CD14 receptor bias was further confirmed by using thioglycollate-elicited murine peritoneal macrophages, which have nonfunctional CR3 before activation. Results indicate that either CR3 or CD14 is involved independently in nonopsonic phagocytosis of different P. aeruginosa strains. Clearance of P. aeruginosa from the endobronchial space may be facilitated by nonopsonic phagocytosis, since low levels of opsonins are present. The impact of lung infection with P. aeruginosa may be determined, in part, by the phagocytic receptor that mediates ingestion.
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