Open AccessNONOPSONIC PHAGOCYTOSIS OF PSEUDOMONAS AERUGINOSA: INSIGHTS FROM AN INFANT WITH LEUKOCYTE ADHESION DEFICIENCY
Author(s) -
Andrew J. Pollard,
John-Paul Heale,
Angela Tsang,
Bonnie G. Massing,
David P. Speert
Publication year - 2001
Publication title -
the pediatric infectious disease journal/the pediatric infectious disease journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 140
eISSN - 1532-0987
pISSN - 0891-3668
DOI - 10.1097/00006454-200104000-00019
Subject(s) - cd18 , phagocytosis , pseudomonas aeruginosa , opsonin , microbiology and biotechnology , immunology , biology , adhesion , integrin , integrin alpha m , leukocyte adhesion deficiency , cell adhesion molecule , cell adhesion , receptor , chemistry , cell , bacteria , flow cytometry , biochemistry , genetics , organic chemistry
Children with leukocyte adhesion deficiency type I are at risk for overwhelming infection because their neutrophils lack surface beta 2 integrins (CD18/CD11) that normally interact with endothelial cell adhesion molecules and mediate migration to sites of bacterial invasion. In vitro studies of phagocytic cells from an infant with leukocyte adhesion deficiency type I demonstrated that complement receptor 3 (CD18/CD11b) mediates nonopsonic phagocytosis of some Pseudomonas aeruginosa strains and might play a control role in the control of Pseudomonas infections at sites where there are low levels of opsonins.