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| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Rajas, Olga Quirós, Luis M. Ortega, Mara Vazquez-Espinosa, Emma Merayo-Lloves, Jesús Vazquez, Fernando García, Beatriz |
| Abstract | Background Lower respiratory infections are among the top ten causes of death worldwide. Since pathogen to cell adhesion is a crucial step in the infection progress, blocking the interaction between eukaryotic receptors and bacterial ligands may enable the pathogenesis process to be stopped. Cell surface glycosaminoglycans (GAGs) are known to be mediators in the adhesion of diverse bacteria to different cell types, making it of interest to examine their involvement in the attachment of various pathogenic bacteria to lung cells, including epithelial cells and fibroblasts. Methods The function of cell surface GAGs in bacterial adhesion was studied by reducing their levels through inhibiting their biosynthesis and enzymatic degradation, as well as in binding competition experiments with various species of GAGs. The participation of the different bacterial adhesins in attachment was evaluated through competition with two peptides, both containing consensus heparin binding sequences. Blocking inhibition assays using anti-syndecans and the enzymatic removal of glypicans were conducted to test their involvement in bacterial adhesion. The importance of the fine structure of GAGs in the interaction with pathogens was investigated in competition experiments with specifically desulfated heparins. Results The binding of all bacteria tested decreased when GAG levels in cell surface of both lung cells were diminished. Competition experiments with different types of GAGs showed that heparan sulfate chains are the main species involved. Blocking or removal of cell surface proteoglycans evidenced that syndecans play a more important role than glypicans. The binding was partially inhibited by peptides including heparin binding sequences. Desulfated heparins also reduced bacterial adhesion to different extents depending on the bacterium and the sulfated residue, especially in fibroblast cells. Conclusions Taken together, these data demonstrate that the GAG chains of the cell surface are involved in the adhesion of bacterial adhesins to lung cells. Heparan sulfate seems to be the main species implicated, and binding is dependent on the sulfation pattern of the molecule. These data could facilitate the development of new anti-infective strategies, enabling the development of new procedures for blocking the interaction between pathogens and lung cells more effectively. |
| Related Links | https://bmcinfectdis.biomedcentral.com/counter/pdf/10.1186/s12879-017-2418-5.pdf |
| Ending Page | 14 |
| Page Count | 14 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| ISSN | 14712334 |
| DOI | 10.1186/s12879-017-2418-5 |
| Journal | BMC Infectious Diseases |
| Issue Number | 1 |
| Volume Number | 17 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2017-05-02 |
| Access Restriction | Open |
| Subject Keyword | Infectious Diseases Parasitology Medical Microbiology Tropical Medicine Internal Medicine Glycosaminoglycans Pathogenic bacteria Infection Host interaction Lung cells |
| Content Type | Text |
| Resource Type | Article |
| Subject | Infectious Diseases |
| Journal Impact Factor | 3.4/2023 |
| 5-Year Journal Impact Factor | 3.3/2023 |
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