TREM-1 deficiency attenuates RIPK3/MLKL-associated epithelial injury in Klebsiella pneumoniae-induced acute lung injury

Background

Klebsiella pneumoniae (KP)-induced acute lung injury involves excessive myeloid inflammation, epithelial barrier disruption, and inflammatory cell death. Triggering receptor expressed on myeloid cells 1 (TREM-1) amplifies innate immune responses, whereas receptor-interacting protein kinase 3 (RIPK3)/mixed lineage kinase domain-like protein (MLKL) signaling contributes to membrane injury. Their relationship during bacterial lung infection remains incompletely understood.