Rhamnolipids Are Virulence Factors That Promote Early Infiltration of Primary Human Airway Epithelia byPseudomonas aeruginosa
Autor: | Thilo Köhler, Paolo Meda, Jean-Silvain Lacroix, Dorothée Caille, Coralie Canard, Laurence Zulianello |
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Rok vydání: | 2006 |
Předmět: |
Adult
Male Cell Survival Virulence Factors Immunology Virulence Biology medicine.disease_cause Models Biological Microbiology Tight Junctions medicine Animals Humans Letter to the Editor Pathogen Cells Cultured Host cell membrane Pseudomonas aeruginosa Cell Polarity Epithelial Cells Middle Aged Molecular Pathogenesis Epithelium Nasal Mucosa Infectious Diseases medicine.anatomical_structure Paracellular transport Respiratory epithelium Female Parasitology Glycolipids Artifacts Signal Transduction Respiratory tract |
Zdroj: | Infection and Immunity. 74:3134-3147 |
ISSN: | 1098-5522 0019-9567 |
DOI: | 10.1128/iai.01772-05 |
Popis: | The opportunistic bacteriumPseudomonas aeruginosacauses chronic respiratory infections in cystic fibrosis and immunocompromised individuals. Bacterial adherence to the basolateral domain of the host cells and internalization are thought to participate inP. aeruginosapathogenicity. However, the mechanism by which the pathogen initially modulates the paracellular permeability of polarized respiratory epithelia remains to be understood. To investigate this mechanism, we have searched for virulence factors secreted byP. aeruginosathat affect the structure of human airway epithelium in the early stages of infection. We have found that only bacterial strains secreting rhamnolipids were efficient in modulating the barrier function of an in vitro-reconstituted human respiratory epithelium, irrespective of their release of elastase and lipopolysaccharide. In contrast to previous reports, we document thatP. aeruginosawas not internalized by epithelial cells. We further report that purified rhamnolipids, applied on the surfaces of the epithelia, were sufficient to functionally disrupt the epithelia and to promote the paracellular invasion of rhamnolipid-deficientP. aeruginosa. The mechanism involves the incorporation of rhamnolipids within the host cell membrane, leading to tight-junction alterations. The study provides direct evidence for a hitherto unknown mechanism whereby the junction-dependent barrier of the respiratory epithelium is selectively altered by rhamnolipids. |
Databáze: | OpenAIRE |
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