Diabetes-associated lung physiology shapes Klebsiella pneumoniae infection dynamics

In leptin receptor-deficient (db/db) mice with type 2 diabetes, Klebsiella pneumoniae establishes larger initial lung founding populations, yielding increased bacterial burdens despite strong cytokine responses.

• Why it matters: Type 2 diabetes mellitus increases susceptibility to bacterial pneumonia, but how diabetic lung physiology affects pathogen establishment is not well defined.
• What they did: After acute lung infection, db/db mice showed higher bacterial burdens and elevated pulmonary vascular endothelial growth factor, alongside BALF metabolite shifts enriched for amino acids; K. pneumoniae grew better in this BALF, and a glutamate-auxotrophic mutant had improved fitness.
• The result: A barcoded K. pneumoniae library revealed significantly larger initial founding populations in db/db lungs, with proportionally wider lung infection bottlenecks and similar founding increases in the liver, linking founding size to pneumonia susceptibility in T2DM.

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