About: Cutting edge: myeloid differentiation factor 88 deficiency improves resistance against sepsis caused by polymicrobial infection

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About: Cutting edge: myeloid differentiation factor 88 deficiency improves resistance against sepsis caused by polymicrobial infection Goto Sponge NotDistinct Permalink

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scientific article published on 01 September 2002

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rdf:type	Item
description	wetenschappelijk artikel (nl) наукова стаття, опублікована у вересні 2002 (uk) article scientifique publié en 2002 (fr) im September 2002 veröffentlichter wissenschaftlicher Artikel (de) artículu científicu espublizáu en setiembre de 2002 (ast) scientific article published on 01 September 2002 (en)
publication date	wds:Q74754482-1719E0D8-2EA2-4B42-8026-81FA266E9FC6
publication date	2002-09-01 00:00:00Z (xsd:dateTime)
language of work or name	wds:Q74754482-B968D1AC-E589-41F5-B4FA-A220FF6E47A8
language of work or name	English
cites work	wds:Q74754482-21317CD4-CC9C-44D7-ACE9-6E72D31E0CD8
cites work	Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene
author name string	wds:Q74754482-66073EFA-DF16-4735-9CCD-85FF69B94FF5 wds:Q74754482-6B6746B8-5029-496B-BA32-13C8DDFF0267 wds:Q74754482-ACF6EE82-755B-4AA7-84FF-0F50C39486EB wds:Q74754482-E1703F6D-DDA8-43B9-8F7B-0A9B7A854BB5
author name string	Bernhard Holzmann Ramunas M Vabulas Heike Weighardt Simone Kaiser-Moore
rdfs:label	Cutting edge: myeloid differentiation factor 88 deficiency improves resistance against sepsis caused by polymicrobial infection (en) Cutting edge: myeloid differentiation factor 88 deficiency improves resistance against sepsis caused by polymicrobial infection (nl)
skos:prefLabel	Cutting edge: myeloid differentiation factor 88 deficiency improves resistance against sepsis caused by polymicrobial infection (en) Cutting edge: myeloid differentiation factor 88 deficiency improves resistance against sepsis caused by polymicrobial infection (nl)
name	Cutting edge: myeloid differentiation factor 88 deficiency improves resistance against sepsis caused by polymicrobial infection (en) Cutting edge: myeloid differentiation factor 88 deficiency improves resistance against sepsis caused by polymicrobial infection (nl)
author	wds:Q74754482-842CB42F-BE0B-4986-AD43-0F790B576DB4 wds:Q74754482-C799081F-B187-4848-A195-189ED013A73B
author	Carsten J Kirschning Hermann Wagner
title	wds:Q74754482-4C4D38E6-C082-4E85-AD35-C9E683BA095E
title	Cutting edge: myeloid differentiation factor 88 deficiency improves resistance against sepsis caused by polymicrobial infection (en)
page(s)	wds:Q74754482-8C4FB0DC-08B0-40A9-8B6B-E6A214429787
page(s)	2823-2827
instance of	wds:Q74754482-E9CB7370-49E6-46CF-85E2-A8F7035C47B1
instance of	scholarly article
main subject	wds:Q74754482-52986DA4-FDFF-4540-BD6B-FDCF1460CC1D
main subject	sepsis
PubMed ID	wds:Q74754482-36E6E5D2-A4CD-4270-95A0-61AA0141FAF6
PubMed ID	http://rdf.ncbi.nlm.nih.gov/pubchem/reference/12218091
PubMed ID	12218091
published in	wds:Q74754482-D417D3FD-DD85-4927-A55E-E4A1C82AB05D
published in	Journal of Immunology
issue	wds:Q74754482-A837102B-9FA4-40E9-B696-7E9580CE6F7E
volume	wds:Q74754482-3D307185-97A3-46F0-BCEF-9448D95B70EA
issue	6
volume	169
DOI	wds:Q74754482-CAEA7CA8-95A4-4C9D-AA96-0A1216A0B0F1
DOI	http://dx.doi.org/10.4049/JIMMUNOL.169.6.2823
DOI	10.4049/JIMMUNOL.169.6.2823
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q74754482
is cites work of	MyD88 primes macrophages for full-scale activation by interferon-gamma yet mediates few responses to Mycobacterium tuberculosis Sepsis-induced organ failure is mediated by different pathways in the kidney and liver: acute renal failure is dependent on MyD88 but not renal cell apoptosis. The helminth product ES-62 protects against septic shock via Toll-like receptor 4-dependent autophagosomal degradation of the adaptor MyD88 Helminths and their implication in sepsis - a new branch of their immunomodulatory behaviour? Dominant role of the MyD88-dependent signaling pathway in mediating early endotoxin-induced murine ileus Increased inflammation and lethality of Dusp1-/- mice in polymicrobial peritonitis models. Inhibitor of apoptosis protein cIAP2 is essential for lipopolysaccharide-induced macrophage survival MyD88-, but not Nod1- and/or Nod2-deficient mice, show increased susceptibility to polymicrobial sepsis due to impaired local inflammatory response Genetic variability in inflammation pathways and prostate cancer risk The role of Toll-like receptors in renal diseases Gene expression disorders of innate antibacterial signaling pathway in pancreatic cancer patients: implications for leukocyte dysfunction and tumor progression Toll-like receptor 2 is required for inflammatory responses to Francisella tularensis LVS Antagonistic antibody prevents toll-like receptor 2-driven lethal shock-like syndromes Differential expression of Toll-like receptors 2 and 4 in tissues of the human female reproductive tract CC chemokine receptor 2 regulates leukocyte recruitment and IL-10 production during acute polymicrobial sepsis Effects of functional Toll-like receptor-4 mutations on the immune response to human and experimental sepsis Animal models of sepsis: setting the stage Animal models of sepsis and sepsis-induced kidney injury Toll-like receptors 2 and 4 contribute to sepsis-induced depletion of spleen dendritic cells Defective innate immunity predisposes murine neonates to poor sepsis outcome but is reversed by TLR agonists. Chloroquine and inhibition of Toll-like receptor 9 protect from sepsis-induced acute kidney injury Type I interferon signaling in hematopoietic cells is required for survival in mouse polymicrobial sepsis by regulating CXCL10. MyD88 dependent signaling contributes to protective host defense against Burkholderia pseudomallei MyD88 is necessary for neutrophil recruitment in hypersensitivity pneumonitis Toll-like receptor 9 inhibition reduces mortality in polymicrobial sepsis MyD88 signaling is indispensable for primary influenza A virus infection but dispensable for secondary infection Complement factor B is the downstream effector of TLRs and plays an important role in a mouse model of severe sepsis. Modeling sepsis in the laboratory: merging sound science with animal well-being Neutrophil mobilization from the bone marrow during polymicrobial sepsis is dependent on CXCL12 signaling Novel therapeutic strategies based on toll-like receptor signaling MyD88 and Trif signaling play distinct roles in cardiac dysfunction and mortality during endotoxin shock and polymicrobial sepsis. Toll-like receptor signaling pathways--therapeutic opportunities The role of type I interferons in TLR responses. IRF3 contributes to sepsis pathogenesis in the mouse cecal ligation and puncture model. Sepsis Induces Hematopoietic Stem Cell Exhaustion and Myelosuppression through Distinct Contributions of TRIF and MYD88. MyD88-dependent signaling prolongs survival and reduces bacterial burden during pulmonary infection with virulent Francisella tularensis Toll-like receptors and myocardial inflammation Differential Paradigms in Animal Models of Sepsis Expression of type I interferon by splenic macrophages suppresses adaptive immunity during sepsis. The TLR4 +896 polymorphism is not associated with lipopolysaccharide hypo-responsiveness in leukocytes Septic acute kidney injury: molecular mechanisms and the importance of stratification and targeting therapy Gene silencing and overexpression of porcine peptidoglycan recognition protein long isoforms: involvement in beta-defensin-1 expression Staphylococcal enterotoxin A induction of pro-inflammatory cytokines and lethality in mice is primarily dependent on MyD88. Interleukin-18 Facilitates the Early Antimicrobial Host Response toEscherichia coliPeritonitis Aberrant inflammatory response to Streptococcus pyogenes in mice lacking myeloid differentiation factor 88. Multiple roles of Myd88 in the immune response to the plague F1-V vaccine and in protection against an aerosol challenge of Yersinia pestis CO92 in mice Role of LPS in the hepatic microvascular dysfunction elicited by cecal ligation and puncture in mice. Hematopoietic but not endothelial cell MyD88 contributes to host defense during gram-negative pneumonia derived sepsis

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