Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most frequent complications of non-obstructive vesico-uretero-renal reflux (VUR) are segmental renal scars. These scars are confined to segments with intrarenal reflux which are, in addition, exposed to bacterial infection. Primarily, only gaping collecting duct orifices, confined to compound papillae and mainly situated at the kidney poles, allow intrarenal reflux. Scar contraction and obstruction seem to be able to transform closed collecting duct orifices into gaping ones, thereby enlarging the parenchymal area prone to intrarenal reflux and to renal scarring. Contrary to earlier reports, a recent survey has documented that new scars in children develop with significant frequency beyond 5 years of age. There is a greater tendency for scarring to develop with more severe VUR, but new renal scars can develop with all grades of VUR. Early and adequate antibiotic treatment decreases the extent of scarring. The results of experimental studies in which renal scarring developed in piglets with bladder decompensation resulting from intravesical obstruction but without bacterial infection may be relevant to the few children with proximal urethral valves and hypertonic neurogenic bladders but not to the large number with non-neurogenic detrusor instability or detrusor sphincter dyssynergia. Prospective studies have not shown different recurrence rates of urinary tract infections in medically managed compared with surgically managed children. The frequency of acute pyelonephritic attacks decreased significantly after operation.
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PMID:Vesico-uretero-renal reflux and the kidney. 315 45

The epithelial cells that line the renal tubule are sometimes severely injured in the course of inflammatory kidney diseases. These renal tubule epithelial cells (RTECs) express some of the Toll-like receptors (TLRs) of the innate immune system. A number of studies have implicated RTECs, together with bone marrow-derived cells, in triggering an innate immune response to bacterial infection and/or ischemic stress. RTECs expressing TLR4, which recognizes lipopolysaccharide (LPS), contribute to defending the host against ascending urinary tract infections (UTIs) caused by uropathogenic Escherichia coli (UPECs). Activation of TLR2 and TLR4 signaling by endogenous damage-associated molecular patterns controls the inflammatory responses of RTECs and cell apoptosis in kidneys subjected to ischemia/reperfusion (I/R) injury. This review will consider some recent advances in understanding of the role of RTECs in inducing the innate immune response in experimental models of ascending UTIs and renal I/R injury. Arginine vasopressin, which regulates renal water absorption, has been shown to act as a potent modulator of the innate response in collecting duct cells, a preferred intrarenal site for UPEC adhesion. The activation of the mitogen-associated protein kinase ERK1/2 in post-hypoxic RTECs has also been shown to be selectively regulated by TLR2 via the serine-threonine protein phosphatase 5, which is associated with the endoplasmic reticulum resident heat shock protein, gp96, which acts as a master chaperone of TLRs. These findings provide further support for the concept that RTECs are actively involved in triggering the innate immune response, at least in the context of ascending UTIs and I/R injury.
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PMID:Contribution of renal tubule epithelial cells in the innate immune response during renal bacterial infections and ischemia-reperfusion injury. 2058

Urinary tract infections (UTIs) mainly due to uropathogenic Escherichia coli (UPEC) are one of the most frequent complications in kidney-transplanted patients, causing significant morbidity. However, the mechanisms underlying UTI in renal grafts remain poorly understood. Here, we analysed the effects of the potent immunosuppressive agent cyclosporine A (CsA) on the activation of collecting duct cells that represent a preferential site of adhesion and translocation for UPEC. CsA induced the inhibition of lipopolysaccharide- induced activation of collecting duct cells due to the downregulation of the expression of TLR4 via the microRNA Let-7i. Using an experimental model of ascending UTI, we showed that the pretreatment of mice with CsA prior to infection induced a marked fall in cytokine production by collecting duct cells, neutrophil recruitment, and a dramatic rise of bacterial load, but not in infected TLR4-defective mice kidneys. This effect was also observed in CsA-treated infected kidneys, where the expression of Let-7i was increased. Treatment with a synthetic Let-7i mimic reproduced the effects of CsA. Conversely, pretreatment with an anti-Let-7i antagonised the effects of CsA and rescued the innate immune response of collecting duct cells against UPEC. Thus, the utilisation of an anti-Let-7i during kidney transplantation may protect CsA-treated patients from ascending bacterial infection.
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PMID:Cyclosporine A Induces MicroRNAs Controlling Innate Immunity during Renal Bacterial Infection. 2906 56