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Differential Roles of MyD88 and TRIF in Hematopoietic and Resident Cells During Murine Gram-Negative Pneumonia

2012; Oxford University Press; Volume: 206; Issue: 9 Linguagem: Inglês

10.1093/infdis/jis505

1537-6613

Miriam H. P. van Lieshout, Dana C. Blok, Catharina W. Wieland, Alex F. de Vos, Cornelis van ‘t Veer, Tom van der Poll,

Inflammation biomarkers and pathways

Background. Pneumonia is frequently caused by gram-negative pathogens, among which Klebsiella pneumoniae prominently features. Recognition of pathogen-associated molecular patterns by Toll-like receptors (TLRs) is important for an appropriate immune response during infection. TLR signaling can proceed via 2 distinct routes that are dependent on the adaptor proteins Myeloid differentiation primary response gene (88) (MyD88) and TIR-domain-containing adaptor-inducing interferon-β (TRIF). The aim of the study was to determine the relative contribution of MyD88 and TRIF signaling in resident and hematopoietic cells to host defense during pneumonia.