ArticleJournal of the American Society of Nephrology : JASN2018
Endotoxin Preconditioning Reprograms S1 Tubules and Macrophages to Protect the Kidney.
Article in Journal of the American Society of Nephrology : JASN, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Insights from integrative spatial transcriptomics in sepsis-associated acute kidney injury.Nature reviews. Nephrology · 2026Review
- Molecular Mechanisms of Sepsis-Associated Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Review
- Urinary metabolomics analysis of patients with renal tubular dysfunction after PCI surgery.International urology and nephrology · 2025Article
- [Itaconic acid alleviates macrophage PANoptosis in sepsisZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- Progression of Kidney Fibrosis after Sepsis: Underestimated Role of Resident Macrophages and Recruited Monocytes.Journal of the American Society of Nephrology : JASN · 2025Review
- Metabolomics- and proteomics-based multi-omics integration reveals early metabolite alterations in sepsis-associated acute kidney injury.BMC medicine · 2025Article
- The Kidney Precision Medicine Project and Single-Cell Biology of the Injured Proximal Tubule.The American journal of pathology · 2025Review
- Inflammation primes the murine kidney for recovery by activating AZIN1 adenosine-to-inosine editing.The Journal of clinical investigation · 2024Article
- Integrin β1-rich extracellular vesicles of kidney recruit Fn1+ macrophages to aggravate ischemia-reperfusion-induced inflammation.JCI insight · 2024Article
- Inflammation primes the kidney for recovery by activating AZIN1 A-to-I editing.bioRxiv : the preprint server for biology · 2023Article
- A macrophage-endothelial immunoregulatory axis ameliorates septic acute kidney injury.Kidney international · 2023Article
- The signaling pathways and therapeutic potential of itaconate to alleviate inflammation and oxidative stress in inflammatory diseases.Redox biology · 2022Review
- Polyamines and Their Metabolism: From the Maintenance of Physiological Homeostasis to the Mediation of Disease.Medical sciences (Basel, Switzerland) · 2022Review
- Hispidulin Ameliorates Endotoxin-Induced Acute Kidney Injury in Mice.Molecules (Basel, Switzerland) · 2022Article
- Innate Immune Memory and the Host Response to Infection.Journal of immunology (Baltimore, Md. : 1950) · 2022Review
- Multi-Omics Techniques Make it Possible to Analyze Sepsis-Associated Acute Kidney Injury Comprehensively.Frontiers in immunology · 2022Review
- Epigenetic memory contributing to the pathogenesis of AKI-to-CKD transition.Frontiers in molecular biosciences · 2022Review
- Integration of spatial and single-cell transcriptomics localizes epithelial cell-immune cross-talk in kidney injury.JCI insight · 2021Article
- The application of omic technologies to research in sepsis-associated acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2021Review
- Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Preconditioning with a low dose of endotoxin confers unparalleled protection against otherwise lethal models of sepsis. The mechanisms of preconditioning have been investigated extensively in isolated immune cells such as macrophages. However, the role of tissue in mediating the protective response generated by preconditioning remains unknown. Here, using the kidney as a model organ, we investigated cell type-specific responses to preconditioning. Compared with preadministration of vehicle, endotoxin preconditioning in the cecal ligation and puncture mouse model of sepsis led to significantly enhanced survival and reduced bacterial load in several organs. Furthermore, endotoxin preconditioning reduced serum levels of proinflammatory cytokines, upregulated molecular pathways involved in phagocytosis, and prevented the renal function decline and injury induced in mice by a toxic dose of endotoxin. The protective phenotype involved the clustering of macrophages around S1 segments of proximal tubules, and full renal protection required both macrophages and renal tubular cells. Using unbiased S1 transcriptomic and tissue metabolomic approaches, we identified multiple protective molecules that were operative in preconditioned animals, including molecules involved in antibacterial defense, redox balance, and tissue healing. We conclude that preconditioning reprograms macrophages and tubules to generate a protective environment, in which tissue health is preserved and immunity is controlled yet effective. Endotoxin preconditioning can thus be used as a discovery platform, and understanding the role and participation of both tissue and macrophages will help refine targeted therapies for sepsis.
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