ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Paneth cell-mediated multiorgan dysfunction after acute kidney injury.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
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- Disruption in glutathione metabolism and altered energy production in the liver and kidney after ischemic acute kidney injury in mice.Scientific reports · 2024Article
- Research progress in the role of gut microbiota in acute kidney injury.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Interorgan communication networks in the kidney-lung axis.Nature reviews. Nephrology · 2024Review
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- IL-6 mediates the hepatic acute phase response after prerenal azotemia in a clinically defined murine model.American journal of physiology. Renal physiology · 2023Article
- Paneth cells as the cornerstones of intestinal and organismal health: a primer.EMBO molecular medicine · 2023Review
- Mineralocorticoid Receptor Antagonism Attenuates Multiple Organ Failure after Renal Ischemia and Reperfusion in Mice.International journal of molecular sciences · 2023Article
- Correlation between perioperative dexmedetomidine administration and postoperative acute kidney injury in hypertensive patients undergoing non-cardiac surgery.Frontiers in pharmacology · 2023Article
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- Multifaceted involvements of Paneth cells in various diseases within intestine and systemically.Frontiers in immunology · 2023Review
- Sepsis and Acute Kidney Injury: A Review Focusing on the Bidirectional Interplay.International journal of molecular sciences · 2022Review
- Mitochondria as mediators of systemic inflammation and organ cross talk in acute kidney injury.American journal of physiology. Renal physiology · 2022Review
- Hyperoxia and Acute Kidney Injury: A Tale of Oxygen and the Kidney.Seminars in nephrology · 2022Review
- Acute Kidney Injury and Gut Dysbiosis: A Narrative Review Focus on Pathophysiology and Treatment.International journal of molecular sciences · 2022Review
- Literature review of the mechanisms of acute kidney injury secondary to acute liver injury.World journal of nephrology · 2022Review
- Intravoxel Incoherent Motion and Dynamic Contrast-Enhanced Magnetic Resonance Imaging to Early Detect Tissue Injury and Microcirculation Alteration in Hepatic Injury Induced by Intestinal Ischemia-Reperfusion in a Rat Model.Journal of magnetic resonance imaging : JMRI · 2021Article
- Selective nanoparticle-mediated targeting of renal tubular Toll-like receptor 9 attenuates ischemic acute kidney injury.Kidney international · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Acute kidney injury (AKI) is frequently complicated by extrarenal multiorgan injury, including intestinal and hepatic dysfunction. In this study, we hypothesized that a discrete intestinal source of proinflammatory mediators drives multiorgan injury in response to AKI. After induction of AKI in mice by renal ischemia-reperfusion or bilateral nephrectomy, small intestinal Paneth cells increased the synthesis and release of IL-17A in conjunction with severe intestinal apoptosis and inflammation. We also detected significantly increased IL-17A in portal and systemic circulation after AKI. Intestinal macrophages appear to transport released Paneth cell granule constituents induced by AKI, away from the base of the crypts into the liver. Genetic or pharmacologic depletion of Paneth cells decreased small intestinal IL-17A secretion and plasma IL-17A levels significantly and attenuated intestinal, hepatic, and renal injury after AKI. Similarly, portal delivery of IL-17A in macrophage-depleted mice decreased markedly. In addition, intestinal, hepatic, and renal injury following AKI was attenuated without affecting intestinal IL-17A generation. In conclusion, AKI induces IL-17A synthesis and secretion by Paneth cells to initiate intestinal and hepatic injury by hepatic and systemic delivery of IL-17A by macrophages. Modulation of Paneth cell dysregulation may have therapeutic implications by reducing systemic complications arising from AKI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.