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      The importance of a beta-glucan receptor in the nonopsonic entry of nontypeable Haemophilus influenzae into human monocytic and epithelial cells.

      The Journal of Infectious Diseases
      Carcinoma, metabolism, Epithelial Cells, Flow Cytometry, Fluorescence, Haemophilus influenzae, Humans, Leukemia, Monocytic, Acute, Lung Neoplasms, Mannose, antagonists & inhibitors, Microscopy, Electron, Monocytes, Platelet Membrane Glycoproteins, Receptors, Cell Surface, Receptors, G-Protein-Coupled, Receptors, Immunologic, Tumor Cells, Cultured

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          Abstract

          Previous reports showed that nontypeable Haemophilus influenzae (NTHi) reside in macrophage-like cells in human adenoid tissue. This study investigated the ability of nonopsonized NTHi and encapsulated H. influenzae type b (Hib) to enter human monocytic and epithelial cells. The number of intracellular bacteria was determined by a viability assay and flow cytometry. To characterize the mechanisms responsible for the internalization of NTHi, different inhibitors of surface molecules, receptor turnover, and the cytoskeleton were used. Hib were found in monocytic cells at very low numbers (<100 bacteria/2x105 cells). In contrast, a great variation in intracellular numbers was detected between the different NTHi isolates (range, 0.0007%-0.28% of the inoculum for monocytes and 0.053%-3.5% for epithelial cells). NTHi entered human monocytic and epithelial cells via a receptor-mediated endocytosis involving mainly a beta-glucan receptor that could be blocked by laminarin.

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