ArticleInfection and immunity2009
Blockade of CD137 signaling counteracts polymicrobial sepsis induced by cecal ligation and puncture.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- CD137L Inhibition Ameliorates Hippocampal Neuroinflammation and Behavioral Deficits in a Mouse Model of Sepsis-Associated Encephalopathy.Neuromolecular medicine · 2023Article
- CD137 Signaling Is Critical in Fungal Clearance during SystemicJournal of fungi (Basel, Switzerland) · 2021Article
- Pretreatment with 6-Gingerol Ameliorates Sepsis-Induced Immune Dysfunction by Regulating the Cytokine Balance and Reducing Lymphocyte Apoptosis.Oxidative medicine and cellular longevity · 2021Article
- Resveratrol attenuates TLR-4 mediated inflammation and elicits therapeutic potential in models of sepsis.Scientific reports · 2020Article
- Toll-like receptor 4 and MAIR-II/CLM-4/LMIR2 immunoreceptor regulate VLA-4-mediated inflammatory monocyte migration.Nature communications · 2014Article
- CD137 expressed on neutrophils plays dual roles in antibacterial responses against Gram-positive and Gram-negative bacterial infections.Infection and immunity · 2013Article
- Blockade of 4-1BB and 4-1BBL interaction reduces obesity-induced skeletal muscle inflammation.Mediators of inflammation · 2013Article
- Bayesian approach to model CD137 signaling in human M. tuberculosis in vitro responses.PloS one · 2013Article
- CD137 deficiency does not affect development of airway inflammation or respiratory tolerance induction in murine models.Clinical and experimental immunology · 2012Article
- CD137 differentially regulates innate and adaptive immunity against Mycobacterium tuberculosis.Immunology and cell biology · 2012Article
- TNF superfamily in inflammatory disease: translating basic insights.Trends in immunology · 2012Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis, a leading cause of death worldwide, involves proinflammatory responses and inefficient bacterial clearance. Previously, we have shown that CD137 (4-1BB), a member of the tumor necrosis factor receptor superfamily, plays critical roles in eradicating infective Listeria monocytogenes, a gram-positive bacterium, and that stimulation of CD137 protects mice from sepsis-induced death. In this study, we unexpectedly found that CD137 activation aggravated polymicrobial sepsis due to mixed gram-positive and gram-negative bacterial infection induced by cecal ligation and puncture (CLP). CD137-deficient (CD137(-/-)) mice showed significantly lower mortality than CD137-sufficient (CD137(+/+)) mice in the CLP model. Administration of an agonistic anti-CD137 monoclonal antibody (MAb) to CD137(+/+) mice decreased their survival in this infection model, while administration of a blocking anti-CD137 ligand MAb (TKS-1) to such mice increased their survival. CD137(-/-) mice and TKS-1-treated CD137(+/+) mice had lower levels of chemokines/proinflammatory cytokines (monocyte chemoattractant protein 1, interleukin-6 [IL-6], tumor necrosis factor alpha, IL-12) and an anti-inflammatory cytokine (IL-10), exhibited improved bacterial clearance in the peritoneum, liver, and blood, and had greater numbers of infiltrated peritoneal neutrophils and macrophages in the CLP model than control mice. Our data suggest that CD137 activation aggravates polymicrobial sepsis induced by CLP.
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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.