ArticlemBio2017
Diabetes Exacerbates Infection via Hyperinflammation by Signaling through TLR4 and RAGE.
Article in mBio, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 74 citations in OpenAlex.
- Aerobic Exercise Training Increases Circulating sRAGE in Adults With Type 2 Diabetes: Associations With Sheddase Regulation.Diabetes, obesity & metabolism · 2026Trial
- Advanced Glycation End-Products Contribute to Delayed Diabetic Corneal Epithelial Wound Healing via the TLR4 Signaling.Investigative ophthalmology & visual science · 2026Article
- Trends in genetic and metabolic engineering of Geobacter sulfurreducens for bioelectrochemical systems: a bibliometric analysis.Archives of microbiology · 2026Review
- Simultaneous assessment of stress hyperglycemia ratio and glucose variability to predict all-cause mortality in sepsis patients across different glucose metabolic states: an observational cohort study with interpretable machine learning approach.International journal of surgery (London, England) · 2026Observational
- Connection between Impaired Fasting Glucose or Type 2 Diabetes Mellitus and Sepsis: A 10-Year Observational Data from the National Health Screening Cohort.Diabetes & metabolism journal · 2025Observational
- The dysfunction of complement and coagulation in diseases: the implications for the therapeutic interventions.MedComm · 2024Review
- Review
- Soluble RAGE and skeletal muscle tissue RAGE expression profiles in lean and obese young adults across differential aerobic exercise intensities.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- Development of a Bispecific Antibody Targeting Clinical Isolates of Acinetobacter baumannii.The Journal of infectious diseases · 2023Article
- Enhanced Vulnerability of Diabetic Mice to HypervirulentPathogens (Basel, Switzerland) · 2023Article
- RAGE-TLR4 Crosstalk Is the Key Mechanism by Which High Glucose Enhances the Lipopolysaccharide-Induced Inflammatory Response in Primary Bovine Alveolar Macrophages.International journal of molecular sciences · 2023Article
- Comorbidities, multimorbidity and COVID-19.Nature medicine · 2023Review
- Knockdown of lncRNA TUG1 alleviates diabetic retinal vascular dysfunction through regulating miR-524-5p/FGFR2.Bioengineered · 2022Article
- Modulation of Gut Microbiota Metabolism in Obesity-Related Type 2 Diabetes Reduces Osteomyelitis Severity.Microbiology spectrum · 2022Article
- Gastrin producing syngeneic mesenchymal stem cells protect non-obese diabetic mice from type 1 diabetes.Autoimmunity · 2022Article
- New insights into the role of melatonin in diabetic cardiomyopathy.Pharmacology research & perspectives · 2022Review
- The Correlation Between MicroRNAs and Diabetic Retinopathy.Frontiers in immunology · 2022Review
- Probiotic induced synthesis of microbiota polyamine as a nutraceutical for metabolic syndrome and obesity-related type 2 diabetes.Frontiers in endocrinology · 2022Review
- Monoclonal Antibody Requires Immunomodulation for Efficacy Against Acinetobacter baumannii Infection.The Journal of infectious diseases · 2021Article
- Notoginsenoside R1 alleviates high glucose-induced inflammation and oxidative stress in HUVECs via upregulating miR-147a.The Kaohsiung journal of medical sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
For more than a century, diabetic patients have been considered immunosuppressed due to defects in phagocytosis and microbial killing. We confirmed that diabetic mice were hypersusceptible to bacteremia caused by Gram-negative bacteria (GNB), dying at inocula nonlethal to nondiabetic mice. Contrary to the pervasive paradigm that diabetes impedes phagocytic function, the bacterial burden was no greater in diabetic mice despite excess mortality. However, diabetic mice did exhibit dramatically increased levels of proinflammatory cytokines in response to GNB infections, and immunosuppressing these cytokines with dexamethasone restored their resistance to infection, both of which are consistent with excess inflammation. Furthermore, disruption of the receptor for advanced glycation end products (RAGE), which is stimulated by heightened levels of AGEs in diabetic hosts, protected diabetic but not nondiabetic mice from GNB infection. Thus, rather than immunosuppression, diabetes drives lethal hyperinflammation in response to GNB by signaling through RAGE. As such, interventions to improve the outcomes from GNB infections should seek to suppress the immune response in diabetic hosts.
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What OpenQuestion holds
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.