ArticleAmerican journal of physiology. Renal physiology2009
Lipopolysaccharide directly alters renal tubule transport through distinct TLR4-dependent pathways in basolateral and apical membranes.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Emerging trends and focus of Toll-like receptors in kidney diseases: a 20-year bibliometric analysis.Frontiers in medicine · 2025Pooled it
- Evaluating the lipid accumulation product index as a predictor for kidney stone prevalence: insights from NHANES 2007-2018.International urology and nephrology · 2024Observational
- Potential Alternative Receptors for SARS-CoV-2-Induced Kidney Damage: TLR-4, KIM-1/TIM-1, and CD147.Frontiers in bioscience (Landmark edition) · 2024Review
- Toll-like Receptor 4 in Acute Kidney Injury.International journal of molecular sciences · 2023Review
- Responses to Ang II (Angiotensin II), Salt Intake, and Lipopolysaccharide Reveal the Diverse Actions of TNF-α (Tumor Necrosis Factor-α) on Blood Pressure and Renal Function.Hypertension (Dallas, Tex. : 1979) · 2022Review
- Innovations and Emerging Therapies to Combat Renal Cell Damage: NADAntioxidants & redox signaling · 2021Review
- Hypothetical Mechanism of Exercise-Induced Acute Kidney Injury Associated with Renal Hypouricemia.Biomedicines · 2021Review
- Sepsis-Associated Acute Kidney Injury.Critical care clinics · 2021Review
- Lipopolysaccharide directly inhibits bicarbonate absorption by the renal outer medullary collecting duct.Scientific reports · 2020Article
- Monophosphoryl lipid A pretreatment suppresses sepsis- and LPS-induced proinflammatory cytokine production in the medullary thick ascending limb.American journal of physiology. Renal physiology · 2020Article
- Acidosis induces antimicrobial peptide expression and resistance to uropathogenicAmerican journal of physiology. Renal physiology · 2020Article
- Loss of Rictor in tubular cells exaggerates lipopolysaccharide induced renal inflammation and acute kidney injury via Yap/Taz-NF-κB axis.Cell death discovery · 2020Article
- Acute kidney injury from sepsis: current concepts, epidemiology, pathophysiology, prevention and treatment.Kidney international · 2019Review
- Monophosphoryl lipid A induces protection against LPS in medullary thick ascending limb through induction of Tollip and negative regulation of IRAK-1.American journal of physiology. Renal physiology · 2019Article
- Innovative Drugs to Target Renal Inflammation in Sepsis: Alkaline Phosphatase.Frontiers in pharmacology · 2019Review
- Monophosphoryl lipid A prevents impairment of medullary thick ascending limb [Formula: see text] absorption and improves plasma [Formula: see text] concentration in septic mice.American journal of physiology. Renal physiology · 2018Article
- Monophosphoryl lipid A induces protection against LPS in medullary thick ascending limb through a TLR4-TRIF-PI3K signaling pathway.American journal of physiology. Renal physiology · 2017Article
- Sepsis-induced acute kidney injury.Current opinion in critical care · 2016Review
- Article
- High-mobility group box 1 inhibits HCO3- absorption in the medullary thick ascending limb through RAGE-Rho-ROCK-mediated inhibition of basolateral Na+/H+ exchange.American journal of physiology. Renal physiology · 2016Article
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Abstract
Bacterial infection of the kidney is associated with renal tubule dysfunction and dysregulation of systemic electrolyte balance. Whether bacterial molecules directly affect renal tubule transport is unknown. We examined the effects of LPS on HCO3(-) absorption in the isolated rat and mouse medullary thick ascending limb (MTAL). LPS decreased HCO3(-) absorption when added to bath or lumen. The MEK/ERK inhibitor U0126 eliminated inhibition by bath LPS but had no effect on inhibition by lumen LPS. Conversely, the mammalian target of rapamycin (mTOR) inhibitor rapamycin eliminated inhibition by lumen LPS but had no effect on inhibition by bath LPS. Inhibiting basolateral Na(+)/H(+) exchange with amiloride eliminated inhibition of HCO3(-) absorption by lumen but not bath LPS. Confocal immunofluorescence showed expression of TLR4 in basolateral and apical membrane domains. Inhibition of HCO3(-) absorption by bath and lumen LPS was eliminated in MTALs from TLR4(-/-) mice. Thus LPS inhibits HCO3(-) absorption through distinct TLR4-dependent pathways in basolateral and apical membranes. These results establish that bacterial molecules can directly impair the transport function of renal tubules, identifying a new mechanism contributing to tubule dysfunction during bacterial infection. The LPS-induced reduction in luminal acidification may contribute to Gram-negative pathogenicity by promoting bacterial adherence and growth and impairing correction of infection-induced systemic acid-base disorders.
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