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Surfactant protein D‐coated Klebsiella pneumoniae stimulates cytokine production in mononuclear phagocytes
Author(s) -
Keisari Yona,
Wang Hongbin,
Mesika Adi,
Matatov Robert,
Nissimov Liat,
Crouch Erika,
Ofek Itzhak
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.70.1.135
Subject(s) - biology , microbiology and biotechnology , klebsiella pneumoniae , innate immune system , cytokine , monocyte , mannose receptor , antibody opsonization , macrophage , opsonin , surfactant protein a , mannose , immune system , immunology , phagocytosis , gene , in vitro , escherichia coli , biochemistry , pulmonary surfactant
Encapsulated Klebsiella pneumoniae strains K21a, K10, and K50, all of which contain dimannose sequences in their capsular polysaccharides that are recognized by the mannose receptor of macrophages, stimulated interleukin secretion and cytokine mRNA expression by human monocyte‐derived macrophages. By contrast, the corresponding unencapsulated phase variants and the K2 strain, which lack the dimannose sequence, did not. Coating of unencapsulated phase variants of Klebsiella strains with surfactant protein (SP)‐D resulted in marked stimulation of cytokine mRNA accumulation. The induction of cytokine mRNA via the mannose receptor occurred only in monocyte‐derived macrophages, whereas that caused by SP‐D‐coated Klebsiella strains occurred in both macrophages and peripheral‐blood monocytes.The results suggested that innate immunity against pulmonary pathogens might be mediated by SP‐D, which acts as an opsonin to enhance the interaction of macrophages with unencapsulated phase variants originating from the upper respiratory tract, and by macrophage mannose receptors, which recognize encapsulated variants expressing capsular dimannose residues.