Kira L. Tomlinson

TL;DR: It is demonstrated that the combined effect of PTEN and CFTR dysfunction stimulates mitochondrial activity, resulting in excessive release of succinate and reactive oxygen species, which promotes the colonization of the airway by Pseudomonas aeruginosa and stimulated an anti-inflammatory host response dominated by immune-responsive gene 1 (IRG1 and itaconate).

TL;DR: It is shown that, in contrast to Gram-negative pathogens, S. aureus induces a distinct airway immunometabolic response dominated by the release of the electrophilic metabolite, itaconate, which adapts to theItaconate-dominated immunometabolism by producing biofilms, which are associated with chronic infection of the human airway.

TL;DR: Investigation of how MRSA adapts to the human airway to establish chronic infection, as occurs during cystic fibrosis, found that selected metabolites may be useful therapeutically to inhibit infection.

TL;DR: In this article, the authors discuss the main differences in the host immunometabolic response to Pseudomonas aeruginosa and Staphylococcus aureus, as well as how these pathogens alter their own metabolism to adapt to airway metabolites and cause persistent lung infections.

TL;DR: In this paper , the authors demonstrate that S. aureus impairs neutrophil function by triggering the production of the anti-inflammatory metabolite itaconate, which impairs survival and bacterial killing.