Differential binding of Haemophilus influenzae to human tissues by fimbriae

Departments of Medical Microbiology, University of Amsterdam, Academic Medical Centre, Meibergdreef 15, NL-1105, AZ Amsterdam, The Netherlands Departments of Pathology, University of Amsterdam, Academic Medical Centre, Meibergdreef 15, NL-1105, AZ Amsterdam, The Netherlands Correspondence should be...

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Published inJournal of medical microbiology Vol. 35; no. 3; pp. 129 - 138
Main Authors STERK, L. M. T, VAN ALPHEN, L, GEELEN-VAN DEN BROEK, L, HOUTHOFF, H. J, DANKERT, J
Format Journal Article
LanguageEnglish
Published Reading Soc General Microbiol 01.09.1991
Society for General Microbiology
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Summary:Departments of Medical Microbiology, University of Amsterdam, Academic Medical Centre, Meibergdreef 15, NL-1105, AZ Amsterdam, The Netherlands Departments of Pathology, University of Amsterdam, Academic Medical Centre, Meibergdreef 15, NL-1105, AZ Amsterdam, The Netherlands Correspondence should be sent to Dr L. van Alphen. Received September 25, 1990 Accepted December 8, 1990 Summary.: The hypothesis was investigated that tissue tropism of Haemophilus influenzae during colonisation and infection is associated with the ability of fimbriate bacteria to bind to the organs and cell types involved. H. influenzae type b with fimbriae (strain 770235f + ) bound to several cell types, including ciliated columnar epithelial cells, pneumocytes, ependymal cells, glial cells, connective tissue fibroblasts, synovial cells, antigen-presenting cells, lymphocytes, erythrocytes and endothelial cells. Binding of H. influenzae to kidney, liver and conjunctiva cells was poor. Fimbriae-specific monoclonal antibody (MAb 6HE8) inhibited this binding. Some binding to endothelial cells and macrophages was also observed with non-fimbriate strains. This binding was not inhibited by MAb 6HE8. We conclude that in-vitro binding of fimbriate H. influenzae is mainly to those tissues and cells where H. influenzae is found during colonisation and infection. The data suggest that a shift to the nonfimbriate form is required for bacteria in the bloodstream to escape clearance mechanisms mediated by blood cells.
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ISSN:0022-2615
1473-5644
DOI:10.1099/00222615-35-3-129