The Binding of Pseudomonas aeruginosa to Cystic Fibrosis Bronchial Epithelial Model Cells Alters the Composition of the Exosomes They Produce Compared to Healthy Control Cells.
Víctor Lozano-IturbeNoelia BlancoEmma Vázquez-EspinosaIvan Fernandez-VegaJesús Merayo-LlovesFernando VazquezRosa M GirónLuis M QuirósPublished in: International journal of molecular sciences (2024)
Cystic fibrosis (CF) is a genetic disease that causes dehydration of the surface of the airways, increasing lung infections, most frequently caused by Pseudomonas aeruginosa . Exosomes are nanovesicles released by cells that play an essential role in intercellular communication, although their role during bacterial infections is not well understood. In this article, we analyze the alterations in exosomes produced by healthy bronchial epithelial and cystic fibrosis cell lines caused by the interaction with P. aeruginosa . The proteomic study detected alterations in 30% of the species analyzed. In healthy cells, they mainly involve proteins related to the extracellular matrix, cytoskeleton, and various catabolic enzymes. In CF, proteins related to the cytoskeleton and matrix, in addition to the proteasome. These differences could be related to the inflammatory response. A study of miRNAs detected alterations in 18% of the species analyzed. The prediction of their potential biological targets identified 7149 genes, regulated by up to 7 different miRNAs. The identification of their functions showed that they preferentially affected molecules involved in binding and catalytic activities, although with differences between cell types. In conclusion, this study shows differences in exosomes between CF and healthy cells that could be involved in the response to infection.
Keyphrases
- cystic fibrosis
- pseudomonas aeruginosa
- induced apoptosis
- cell cycle arrest
- stem cells
- inflammatory response
- lung function
- endoplasmic reticulum stress
- genome wide
- dna methylation
- escherichia coli
- biofilm formation
- single cell
- acinetobacter baumannii
- drug resistant
- multidrug resistant
- binding protein
- air pollution
- cell proliferation