Staphylococcus aureus products subvert the Burkholderia cenocepacia-induced inflammatory response in airway epithelial cells
| Autor: | Yuan Ji, Malcolm L. Watson, Albert Bolhuis |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Microbiology (medical) MAPK/ERK pathway Staphylococcus aureus Burkholderia cenocepacia 030106 microbiology Inflammation medicine.disease_cause Microbiology 03 medical and health sciences Immune system Western blot medicine medicine.diagnostic_test biology Effector Burkholderia cepacia complex Interleukin General Medicine biology.organism_classification immunomodulatory products 030104 developmental biology medicine.symptom host–pathogen interactions |
| Zdroj: | Ji, Y, Bolhuis, A & Watson, M L 2019, ' Staphylococcus aureus products subvert the Burkholderia cenocepacia-induced inflammatory response in airway epithelial cells ', Journal of Medical Microbiology, vol. 68, no. 12, pp. 1813-1822 . https://doi.org/10.1099/jmm.0.001100 |
| ISSN: | 1473-5644 0022-2615 |
| DOI: | 10.1099/jmm.0.001100 |
| Popis: | Introduction. Chronic pulmonary infection is associated with colonization with multiple micro-organisms but host-microbe and microbe-microbe interactions are poorly understood.Aim. This study aims to investigate the differences in host responses to mono- and co-infection with S. aureus and B. cenocepacia in human airway epithelial cells.Methodology. We assessed the effect of co-infection with B. cenocepacia and S. aureus on host signalling and inflammatory responses in the human airway epithelial cell line 16HBE, using ELISA and western blot analysis.Results. The results show that B. cenocepacia activates MAPK and NF-κB signalling pathways, subsequently eliciting robust interleukin (IL)-8 production. However, when airway epithelial cells were co-treated with live B. cenocepacia bacteria and S. aureus supernatants (conditioned medium), the pro-inflammatory response was attenuated. This anti-inflammatory effect was widely exhibited in the S. aureus isolates tested and was mediated via reduced MAPK and NF-κB signalling, but not via IL-1 receptor or tumour necrosis factor receptor modulation. The staphylococcal effectors were characterized as small, heat-stable, non-proteinaceous and not cell wall-related factors.Conclusion. This study demonstrates for the first time the host response in a S. aureus/B. cenocepacia co-infection model and provides insight into a staphylococcal immune evasion mechanism, as well as a therapeutic intervention for excessive inflammation. |
| Databáze: | OpenAIRE |
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