Mesenchymal Stromal Cell Extracellular Vesicles Reduce Biofilm Formation, and let-7b-5p Loading Confers Additional Anti-Inflammatory Effects.

Cystic Fibrosis (CF) is a multiorgan disease caused by mutations in the gene, leading to chronic pulmonary infections and hyperinflammation. Among pathogens colonizing the CF lung, is predominant, infecting over 50% of adults with CF, and becoming antibiotic-resistant over time. Current therapies for CF, while providing tremendous benefits, fail to eliminate persistent bacterial infections, chronic inflammation, and irreversible lung damage, necessitating novel therapeutic strategies.

Let-7b-5p loaded Mesenchymal Stromal Cell Extracellular Vesicles reduce -biofilm formation and inflammation in CF Bronchial Epithelial Cells.

Cystic Fibrosis (CF) is a multiorgan disease caused by mutations in the gene, leading to chronic pulmonary infections and hyperinflammation. Among pathogens colonizing the CF lung, is predominant, infecting over 50% of adults with CF, and becoming antibiotic-resistant over time. Current therapies for CF, while providing tremendous benefits, fail to eliminate persistent bacterial infections, chronic inflammation, and irreversible lung damage, necessitating novel therapeutic strategies.

Gene expression responses of CF airway epithelial cells exposed to elexacaftor/tezacaftor/ivacaftor suggest benefits beyond improved CFTR channel function.

The combination of elexacaftor/tezacaftor/ivacaftor (ETI, Trikafta) reverses the primary defect in cystic fibrosis (CF) by improving CFTR-mediated Cl and HCO secretion by airway epithelial cells (AECs), leading to improved lung function and less frequent exacerbations and hospitalizations. However, studies have shown that CFTR modulators like ivacaftor, a component of ETI, have numerous effects on CF cells beyond improved CFTR channel function. Because little is known about the effect of ETI on CF AEC gene expression, we exposed primary human AEC to ETI for 48 h and interrogated the transcriptome by RNA-seq and qPCR.

Bacterial Outer Membrane Vesicles and Immune Modulation of the Host.

This article reviews the role of outer membrane vesicles (OMVs) in mediating the interaction between Gram-negative bacteria and their human hosts. OMVs are produced by a diverse range of Gram-negative bacteria during infection and play a critical role in facilitating host-pathogen interactions without requiring direct cell-to-cell contact. This article describes the mechanisms by which OMVs are formed and subsequently interact with host cells, leading to the transport of microbial protein virulence factors and short interfering RNAs (sRNA) to their host targets, exerting their immunomodulatory effects by targeting specific host signaling pathways.