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• W2126149196 startingPage "4773" @default.
• W2126149196 abstract "Abstract TLR4 plays a central role in resistance to pyelonephritis caused by uropathogenic Escherichia coli (UPEC). It has been suggested that renal tubule epithelial cells expressing TLRs may play a key role in inflammatory disorders and in initiating host defenses. In this study we used an experimental mouse model of ascending urinary tract infection to show that UPEC isolates preferentially adhered to the apical surface of medullary collecting duct (MCD) intercalated cells. UPEC-infected C3H/HeJ (Lpsd) mice carrying an inactivating mutation of tlr4 failed to clear renal bacteria and exhibited a dramatic slump in proinflammatory mediators as compared with infected wild-type C3H/HeOuJ (Lpsn) mice. However, the level of expression of the leukocyte chemoattractants MIP-2 and TNF-α still remained greater in UPEC-infected than in naive C3H/HeJ (Lpsd) mice. Using primary cultures of microdissected Lpsn MCDs that expressed TLR4 and its accessory molecules MD2, MyD88, and CD14, we also show that UPECs stimulated both a TLR4-mediated, MyD88-dependent, TIR domain-containing adaptor-inducing IFN-β-independent pathway and a TLR4-independent pathway, leading to bipolarized secretion of MIP-2. Stimulation by UPECs of the TLR4-mediated pathway in Lpsn MCDs leads to the activation of NF-κB, and MAPK p38, ERK1/2, and JNK. In addition, UPECs stimulated TLR4-independent signaling by activating a TNF receptor-associated factor 2-apoptosis signal-regulatory kinase 1-JNK pathway. These findings demonstrate that epithelial collecting duct cells are actively involved in the initiation of an immune response via several distinct signaling pathways and suggest that intercalated cells play an active role in the recognition of UPECs colonizing the kidneys." @default.
• W2126149196 created "2016-06-24" @default.
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• W2126149196 date "2006-10-01" @default.
• W2126149196 modified "2023-10-17" @default.
• W2126149196 title "Renal Collecting Duct Epithelial Cells React to Pyelonephritis-Associated <i>Escherichia coli</i> by Activating Distinct TLR4-Dependent and -Independent Inflammatory Pathways" @default.
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• W2126149196 doi "https://doi.org/10.4049/jimmunol.177.7.4773" @default.
• W2126149196 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16982918" @default.
• W2126149196 hasPublicationYear "2006" @default.
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