ArticleThe Journal of biological chemistry2011
Delineation of the role of Toll-like receptor signaling during peritonitis by a gradually growing pathogenic Escherichia coli.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 23 citations in OpenAlex.
- Acyl-CoA-binding protein (ACBP): a poor-prognosis biomarker in sepsis and a target for disease mitigation.Signal transduction and targeted therapy · 2026Article
- Deficiencies of carboxypeptidase N and carboxypeptidase B2 have opposite effects in a virulent mouse E. coli sepsis model.Journal of thrombosis and haemostasis : JTH · 2025Article
- Proteomic Profiling of Acoustically Isolated Extracellular Vesicles from Blood Plasma during Murine Bacterial Sepsis.Journal of proteome research · 2025Article
- A pharmacoproteomic landscape of organotypic intervention responses in Gram-negative sepsis.Nature communications · 2023Article
- Bruton's Tyrosine Kinase Deficiency Ameliorates Antimicrobial Host Defense during Peritonitis Induced by Pathogenic Escherichia coli.Infection and immunity · 2022Article
- Age-related decline in the resistance of mice to bacterial infection and in LPS/TLR4 pathway-dependent neutrophil responses.Frontiers in immunology · 2022Article
- Article
- The GPCR adaptor protein norbin suppresses the neutrophil-mediated immunity of mice to pneumococcal infection.Blood advances · 2021Article
- Cathelicidins InhibitJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Expression and Function of Granzymes A and B inMediators of inflammation · 2017Article
- SOCS Proteins as Regulators of Inflammatory Responses Induced by Bacterial Infections: A Review.Frontiers in microbiology · 2017Review
- Assessment of intensive care unit-acquired weakness in young and old mice: An E. coli septic peritonitis model.Muscle & nerve · 2016Article
- Toll-Like Receptor Signalling Is Not Involved in Platelet Response to Streptococcus pneumoniae In Vitro or In Vivo.PloS one · 2016Article
- Abdominal Distension and Escherichia coli Peritonitis in Mice Lacking Myeloid Differentiation Factor 88.Comparative medicine · 2015Article
- Triggering receptor expressed on myeloid cells-2 fine-tunes inflammatory responses in murine Gram-negative sepsis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Differential Toll-Like Receptor-Signalling of Burkholderia pseudomallei Lipopolysaccharide in Murine and Human Models.PloS one · 2015Article
- TIR-Domain-Containing Adaptor-Inducing Interferon-β (TRIF) Mediates Antibacterial Defense during Gram-Negative Pneumonia by Inducing Interferon-x03B3.Journal of innate immunity · 2015Article
- TLR4 inhibition impairs bacterial clearance in a therapeutic setting in murine abdominal sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Limited role of nuclear receptor Nur77 in Escherichia coli-induced peritonitis.Infection and immunity · 2014Article
- Differential response of bovine mammary epithelial cells to Staphylococcus aureus or Escherichia coli agonists of the innate immune system.Veterinary research · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In a mouse model of Escherichia coli sepsis characterized by a primary peritoneal infection with 10(4) E. coli and a gradually growing bacterial load, we here show that the early cytokine response and antibacterial defense are dominated by TLR4 via a cooperative action of MyD88 and Trif. Although MyD88(-/-) mice succumbed earlier than WT mice in this E. coli peritonitis model, Trif(-/-) mice displayed a small but significant survival advantage. Despite a large early deficit in antimicrobial defense, TLR4(-/-) mice showed an unaltered survival with normal neutrophil attraction to the peritoneal cavity and normal or even elevated late cytokine release. TLR2 compensated for the lack of TLR4 because TLR2(-/-)/TLR4(-/-) mice did show decreased neutrophil attraction and increased mortality compared with WT mice. Nearly normal early peritoneal TNFα production and lack of early counterregulating systemic levels of the chemoattractant KC were associated with normal peritoneal neutrophil attraction in TLR4(-/-) mice. Late stage increased TNF, IL-1β, IFN-β, and typical IFN-γ production in TLR4(-/-) mice prompted us to evaluate expression of the negative feedback regulator SOCS-1. Lack of early hepatic SOCS-1 expression in TLR4(-/-) mice explained the late innate production of IFN-γ by the liver in TLR4(-/-) mice in this low dose E. coli peritonitis model. In contrast, early TLR4-induced IFN-γ production is described as a hallmark in high dose E. coli peritonitis models. The present study displays how the kinetics of pro- and anti-inflammatory mechanisms are regulated by TLRs during peritonitis by a gradually growing E. coli load and how these kinetics may affect outcome.
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