|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Combined with our previous in vitro functional study, the results suggest that the TLR4 11367 polymorphism might be a good predictor of who is more likely to develop complications such as sepsis or multiple organ dysfunction syndrome, depending on genotype.
|
20026833 |
2009 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Although TLR-4 mRNA expression in healthy control monocytes could be modulated in vitro by culture with lipopolysaccharide or interleukin-10, this was not observed in monocytes obtained from sepsis and ITU control subjects, suggesting that septic and ITU control milieus may alter the immunoregulation of TLR-4 mRNA expression on monocytes.
|
15086396 |
2004 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Freshly isolated PMN from patients with sepsis exhibited significantly (P < 0.05) higher mean fluorescence for TLR-2 (78.0 +/- 18.6) and TLR-4 (11.4 +/- 2.3) than controls (12.8 +/- 2.2 and 2.3 +/- 0.4).
|
15489631 |
2004 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Furthermore, the identification of platelet TF and TLR4 as regulators of the effect of E. coli O111 might represent a novel therapeutic target to reduce the devastating consequences of the hemostatic disorder during sepsis.
|
28957360 |
2017 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
TLR4 is of particular interest, since over-stimulation of its pathway by excess lipopolysaccharide (LPS) molecules from the outer membranes of Gram-negative bacteria can result in sepsis, which causes millions of deaths each year.
|
31351116 |
2019 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
We adapted template-directed dye-terminator incorporation with fluorescence polarization detection (TDI-FP) to the analysis of eight SNPs implicated in mediating the sepsis syndrome: TNF-alpha (-308), TNF-alpha (-238), TNF-beta (+250), IL-1beta (+3953), IL-6 (-174), IL-10 (-592), plasminogen activator inhibitor-1 (PAI-1 (-675)), and TLR4 299 (+1032).
|
12411588 |
2002 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
The virulence properties demonstrated by Acinetobacter spp. primarily stem from evasion of rapid clearance by the innate immune system, effectively enabling high bacterial density that triggers lipopolysaccharide (LPS)-Toll-like receptor 4 (TLR4)-mediated sepsis.
|
27974412 |
2017 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Allicin Improves Lung Injury Induced by Sepsis via Regulation of the Toll-Like Receptor 4 (TLR4)/Myeloid Differentiation Primary Response 88 (MYD88)/Nuclear Factor kappa B (NF-κB) Pathway.
|
30957795 |
2019 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Because TcpB suppresses both TLR4- and caspase-4/11-mediated inflammation, TcpB might be a candidate target for developing drugs against LPS-induced septicemia.
|
29061850 |
2017 |
|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Specific point mutations in the human toll-like receptor 4 (TLR4) confer altered risk for diverse diseases including sepsis, aspergillosis and inflammatory bowel disease.
|
30885307 |
2019 |
|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
To simulate sepsis, male C57BL/6 (wild-type) and C57BL/10ScNJNJU (TLR4<sup>-/-</sup>) mice were subjected to cecal ligation and puncture (CLP).
|
29149705 |
2018 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Toll receptors and sepsis.
|
11805536 |
2001 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Alkaline phosphatase (AP) is currently being investigated as an anti-inflammatory agent for detoxifying LPS through dephosphorylating lipid A, thus providing a potential treatment for managing both acute (sepsis) and chronic (metabolic endotoxemia) pathologies wherein aberrant TLR4/MD2 activation has been implicated.
|
31704704 |
2019 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Taken together, the present results suggested that apelin had a protective effect against sepsis‑induced cardiac impairment by attenuating TLR4 and NLRP3 signaling‑mediated inflammatory responses.
|
29749463 |
2018 |
|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Serum levels of tumour necrosis factor, interleukin (IL)-10, and IL-6 at sepsis onset did not significantly differ between patients carrying wild-type and mutant TLR4.
|
12807489 |
2003 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Myeloid differentiation 2 (MD2) is essential to the recognition of lipopolysaccharide (LPS) and the subsequent mediation of toll-like receptor 4 (TLR4)-dependent acute inflammatory disorders including sepsis and acute lung injury.
|
28858767 |
2017 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Activation of the TLR4 receptor by bacterial lipopolysaccharide (LPS) is the most widely studied TLR pathway due to its central role in host responses to gram-negative bacterial infection and its contribution to endotoxemia and sepsis.
|
28248930 |
2017 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Increased TLR4 Expression Aggravates Sepsis by Promoting IFN-<i>γ</i> Expression in CD38<sup>-/-</sup> Mice.
|
30915370 |
2019 |
|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Our study investigated the association between TLR4 mutations (Asp299Gly and Thr399Ile) and CD14 polymorphism(s) with outcome in an intensive care unit (ICU) population at risk for sepsis.
|
12404174 |
2002 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
In vivo, ES-62 protected mice against endotoxic and polymicrobial septic shock by TLR4-mediated induction of autophagy and was protective even when administered after the induction of sepsis.
|
21358639 |
2011 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our results indicate that TFAM repairs mtDNA by blocking the TLR4/ROS/P38MAPK signaling pathway in inflammatory cells, thereby repairing septic tubular epithelial cells, and TFAM may serve as a new target for sepsis therapy.
|
31430762 |
2019 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Highlights of this study include: human SAA is possibly only expressed in a subset of septic patients; SAA induces HMGB1 release via TLR4 and RAGE receptors; SAA supplementation worsens the outcome of lethal endotoxemia; whereas SAA-neutralizing antibodies confer protection against lethal endotoxemia and sepsis.
|
26052716 |
2015 |
|
Septicemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Candidate genes for asthma and allergic diseases co-associated with sepsis including innate immunity receptors and related molecules (CD14, TLR4 and AOAH) and novel genes such as MYLK provide good examples of pleitropic effects of innate immunity genes, where variants conferring risk to specific traits (i.e. sepsis) under one set of genetic and environmental circumstances confer a reduced risk in a different (but possibly related) clinical outcome (i.e. allergic asthma), and support the 'common variant/multiple disease' hypothesis.
|
17989521 |
2007 |
|
Septicemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Transfer of a normal microbiota into antibiotic-treated neonates induced IL-17 production by group 3 innate lymphoid cells (ILCs) in the intestine, increasing plasma G-CSF levels and neutrophil numbers in a Toll-like receptor 4 (TLR4)- and myeloid differentiation factor 88 (MyD88)-dependent manner and restored IL-17-dependent resistance to sepsis.
|
24747744 |
2014 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
We find the Cpb1-C3-C3aR pathway induces caspase-11 expression through amplification of MAPK activity downstream of TLR4 and Ifnar activation, and mediates severity of LPS-induced sepsis (endotoxemia) and disease outcome in mice.
|
27697835 |
2016 |