Lipopolysaccharide-Binding Protein Increases Toll-like Receptor 4–Dependent Activation by Nontypeable Haemophilus influenzae

• Published in: The Journal of infectious diseases Vol. 184; no. 7; pp. 926 - 930
• Main Authors: Ahrén, Irini Lazou, Bjartell, Anders, Egesten, Arne, Riesbeck, Kristian
• Format: Journal Article
• Language: English
• Published: Chicago, IL The University of Chicago Press 01.10.2001; University of Chicago Press; Oxford University Press
• Subjects: Acute-Phase Proteins - pharmacology; Animals; Bacteria; Bacteriology; Biological and medical sciences; Carrier Proteins - pharmacology; Cell Line; Cell lines; Cell receptors; Cell structures and functions; CHO Cells; Clinical Medicine; Concise Communications; Cricetinae; Cytokines; Dose-Response Relationship, Drug; Drosophila Proteins; Epithelial cells; Fundamental and applied biological sciences. Psychology; Haemophilus influenzae; Haemophilus influenzae - growth & development; Haemophilus influenzae - metabolism; Hepatocytes; Humans; Infectious Medicine; Infektionsmedicin; Klinisk medicin; Lipopolysaccharide Receptors - genetics; lipopolysaccharide-binding protein; Low back pain; Medical and Health Sciences; Medicin och hälsovetenskap; Membrane Glycoproteins - drug effects; Membrane Glycoproteins - genetics; Membrane Glycoproteins - metabolism; Microbiology; Miscellaneous; Molecular and cellular biology; Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains; Protein Binding; Receptors, Cell Surface - drug effects; Receptors, Cell Surface - genetics; Receptors, Cell Surface - metabolism; Signal Transduction - drug effects; Toll like receptors; Toll-Like Receptor 2; Toll-Like Receptor 4; Transfection; Pasteurellaceae; Flow cytometry; Binding protein; Pulmonary alveolus; Lipopolysaccharide; Bacteria; Epithelial cell; Concentrate; Respiratory system; Haemophilus influenzae; Macrophage
• ISSN: 0022-1899; 1537-6613; 1537-6613
• DOI: 10.1086/323398

Nontypeable Haemophilus influenzae (NTHi) is a common cause of respiratory tract infections. This study investigated the ability of NTHi to bind lipopolysaccharide-binding protein (LBP) derived from respiratory epithelial cells and the subsequent stimulation of transfected cells expressing membrane-bound CD14 and toll-like receptor 2 (TLR2) or TLR4. In the absence of LBP, NTHi at high concentrations (100 bacteria/epithelial cell) were required to induce signals through TLR2 and TLR4. Flow cytometry showed that NTHi in the stationary phase bound more LBP than did log-phase bacteria. Of interest, as few as 1 LBP-bearing bacterium/cell induced strong signaling through TLR4. In contrast, LBP bound to NTHi did not promote any increased signaling mediated by TLR2, compared with NTHi without LBP. These data suggest that, upon NTHi infection, low numbers of bacteria binding LBP may activate TLR4-bearing cells, such as alveolar macrophages, and consequently induce an inflammatory response