Urinary tract infection and pyelonephritis are mainly due to uropathogenic Escherichia coli (UPEC), and are common infectious diseases that constitute a significant cause of morbidity and mortality in humans. They are also the most frequent infectious complications in renal transplant patients, and can impair long-term renal graft function and outcome. UPEC may invade the kidneys via the systemic circulation or by local retrograde infection. They induce the proinflammatory mediators, which are intended to defend the host and clear bacteria from the kidneys. The Toll-like receptors (TLRs) play a key role in the recognition of bacterial components and in inducing the inflammatory response that is mediated by various intracellular signaling pathways. To date, 13 TLRs have been identified in mammals. Recent studies have provided evidence sug- Prof. Alain Vandewalle gesting that renal tubule epithelial cells express most of the TLRs initially identified in bone marrow-derived cells. Murine renal tubule cells express TLR1, 2, 3, 4, 6, and 11. TLR4, which recognizes lipopolysaccharide (LPS), the main constituent of Gram-negative bacteria, plays a key role in inducing the inflammatory responses elicited by UPEC. This review will consider some aspects of TLR function in the kidney, particularly in the renal tubule epithelial cells, and the role of these receptors in enabling the body to cope with urinary tract infections and pyelonephritis caused by UPECs.