NAD metabolism is a key modulator of bacterial respiratory epithelial infections.

Lower respiratory tract infections caused by Streptococcus pneumoniae (Spn) are a leading cause of death globally. Here we investigate the bronchial epithelial cellular response to Spn infection on a transcriptomic, proteomic and metabolic level. We found the NAD salvage pathway to be dysregulated upon infection in a cell line model, primary human lung tissue and in vivo in rodents, leading to a reduced production of NAD.

Streptococcus pneumoniae disrupts the structure of the golgi apparatus and subsequent epithelial cytokine response in an HO-dependent manner.

Background: Lung infections caused by Streptococcus pneumonia are a global leading cause of death. The reactive oxygen species HO is one of the virulence factors of Streptococcus pneumoniae. The Golgi apparatus is essential for the inflammatory response of a eukaryotic cell.

Antibacterial activity of a defensin in an infection model of .

() is the most common bacterial cause of community-acquired pneumonia. Increasing rates of antibiotic-resistant strains impair therapy and necessitate alternative treatment options. In this study, we analysed insect-derived antimicrobial peptides (AMPs) for antibacterial effects on in a human infection model.