|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Because the nuclear factor-κB (NF-κB) coupled pathway is believed to amplify inflammation prevailing in sepsis, the authors tested the hypotheses that the insertion-deletion polymorphism (-94ins/delATTG) (1) alters nuclear translocation of nuclear factor-κB and activator protein-1 (NF-κB1) in monocytes after lipopolysaccharide stimulation; (2) affects lipopolysaccharide-induced NF-κB1 messenger RNA expression, tumor necrosis factor α concentrations, and tissue factor activity; and (3) may be associated with increased 30-day mortality in patients with sepsis.
|
23249930 |
2013 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Here, we demonstrate that omega-9 treatment is associated with increased levels of the anti-inflammatory cytokine IL-10 and decreased levels of the proinflammatory cytokines TNF-<i>α</i> and IL-1<i>β</i> in peritoneal lavage fluid of mice with sepsis.
|
30538802 |
2018 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The absence of TRPM2 triggered less production of inflammatory mediators (IL-1β, IL-6, TNF-α) and decreased apoptosis related proteins (BNIP3, AIF, Endo G) expressions in response to LPS induced sepsis.
|
31450153 |
2019 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
To support the coordination of bioenergetics in human sepsis, we observed elevated NAD(+) levels concomitant with SIRT1 and RelB accumulation at the TNF-α promoter of endotoxin tolerant sepsis blood leukocytes.
|
21245135 |
2011 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Sepsis induces the activation of complement factor via 3 pathways and the release of inflammatory cytokines such as tumor necrosis factor alpha (TNF-α) and interleukin-1beta (IL-1β), resulting in a systemic inflammatory response.
|
28525674 |
2017 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The results of the in vitro and in vivo experiments indicated that the levels of LPS, TNF-α and IL-6 of the palmatine group were significantly lower than those of the sepsis model group (p<0.01).
|
28278436 |
2017 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Nfe2l2(-/-) mice in sepsis also generated higher hepatic TNF-α mRNA levels, lower NRF-1 and PGC-1α mRNA levels, and no enhancement of anti-inflammatory Il10, Socs3, or bcl-x(L) gene expression.
|
21454555 |
2011 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
IL-27 was elevated in sepsis patients with acute hepatic injury, which correlated with the Acute Physiologic Assessment and Chronic Health Evaluation II (APACHEII) scores, Sequential Organ Failure Assessment (SOFA) scores, and procalcitonin, C-reactive protein, IL-6, and TNF-α expression.
|
31786500 |
2020 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Forced expression of CRBN in macrophage of KO mice suppressed activation of 5' adenosine monophosphate-activated protein kinase (AMPK) and HO-1 and augmented expression of TNF-α and HMGB1 as inhibition of AMPK by compound C. These studies demonstrate the contribution of CRBN expression to the pathogenesis of CLP-induced sepsis and peritoneal macrophage responses and suggest a novel therapeutic modality for polymicrobial sepsis.
|
29170136 |
2018 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Plasma levels of miR-187 in sepsis patients were inversely correlated with those of TNF-α and IL-6 (r = -0.2841, -0.2163), and plasma levels of miR-21 and miR-145 were positively correlated with those of TNF-α and IL-6 (r = 0.615, 0.3057, 0.4465, 0.2734).
|
31415369 |
2019 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Therapy with vitamin D in animal models of sepsis improves blood coagulation parameters in disseminated intravascular coagulation and modulates levels of systemic inflammatory cytokines including TNF-α and IL-6.
|
21777617 |
2011 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The levels of TNF-α were higher in patients with sepsis (P=0.03), and deceased patients (P=0.001).
|
31701129 |
2019 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Sepsis induced a generalized up-regulation of both human and murine plasma cytokines (TNFα, IL-6, IL-10, IL-8/KC, MCP-1); it was additionally aggravated in P-DIE vs. P-SUR.
|
31297113 |
2019 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Our findings suggest that TNF-alpha-mediated up-regulation of PDE2 may destabilize endothelial barrier function in sepsis.
|
15650061 |
2005 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The progression of OPG levels paralleled the deterioration of kidney and endothelial functions from sepsis to sepsis-AKI, revealed as progressively increased levels of serum E-selectin (15.3%), endothelin-1 (ET-1) (19.6%), and decreased nitric oxide (NO) (29.7%), associated with elevations of TNF-α (25.5%) and TGF-β (18%).
|
28840836 |
2017 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Tumor necrosis factor-α (TNFα) is a major cytokine that is highly expressed in many diseased conditions, such as inflammatory diseases, sepsis, and cancer.
|
30818829 |
2019 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Therefore, the JNK1 and nNOS inhibitory pathways represent a "brake" that limits myocardial TNF-alpha expression in sepsis.
|
20237583 |
2010 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
T-lymphocyte subsets were detected by flow cytometer, the levels of tumor necrosis factor-α, interleukin-1 and calcitonin were determined by double-antibody immunoluminometric assay, and the effect of vitamin D on the above indicators in the treatment of sepsis was observed.
|
30116318 |
2018 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
BTED for 6 hours significantly reduced the mRNA expression levels of tumor necrosis factor alpha (TNF-α) and IL-1β (all p < 0.05 vs. sepsis group), whereas mRNA expression of TNF-α and IL-1β in the intestine was increased after 6 hours' septic bile infusion compared with normal bile infusion group (all p < 0.05).
|
29847538 |
2018 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Plasma cytokine (IL-1β and TNF-α) levels were increased in patients with sepsis exhibiting high mPR3 expression.
|
29621735 |
2018 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The expression levels of AQP-5 in the sepsis group were significantly decreased compared with those in ctrl and SO groups (P<0.01), while the levels of TNF-α, IL-6 and p-P38 were significantly increased in sepsis group compared with those in ctrl and SO groups (P<0.01).
|
30127927 |
2018 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In summary, this work provides the first in vivo evidence that administering BMMSCs or UCMSCs to rats with CLP-induced sepsis could increase circulating CD3+CD4+CD25+ Treg cells and Treg cells/T cells ratio, enhance Treg cell suppressive function, and decrease serum levels of interleukin-6 and tumor necrosis factor-α, suggesting the immunomodulatory association of Treg cells and MSCs during sepsis.
|
25337817 |
2014 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The protection of female hearts against the dysfunction associated with sepsis is (at least in part) attributable to cardiac activation of the Akt/eNOS survival pathway, decreased activation of NF-κB, and decreased expression of iNOS, TNF-α and IL-6.
|
24945834 |
2014 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
<b>Conclusion:</b> UTI effectively protects TJs and helps to attenuate the permeability of pulmonary capillary endothelial cells during sepsis through inhibiting NF-κB and MAPKs signal pathways and TNF-α expression.
|
30150933 |
2018 |
|
Septicemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
MALAT1 knockdown significantly increased LVSP and +dp/dsmax, decreased LVEDP and -dp/dsmax of sepsis as well as levels of cTn-I, CK, CK-MB, TNF-α, IL-1β, IL-6, IL-10, IL-17, IFN-γ, C5 and C5a.
|
29227823 |
2018 |