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.
A number of pre-clinical studies have shown an auto amplification of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, and IL-6 in the first few hours after sepsis induction, also increased blood-brain barrier permeability, elevated levels of matrix metalloproteinases, increased levels of damage-associated molecular patterns were demonstrated.
This study will provide high-quality synthesis of current evidence of QWBDD in the treatment of sepsis from the following aspects, including 28-day mortality, mean arterial pressure (MAP), blood lactate, procalcitonin (PCT), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), hypersensitive C-reactive protein (hs-CRP), acute physiology and chronic health score (APACHE-II), intensive care unit stay, mean hospital stay, mechanical ventilation time, etc.
Therefore, we hypothesized that TNF has a dual role in sepsis, namely a mediating and a protective role, and that protection might be obtained by TNFR1-specific inhibition.
Whereas it is known that BA metabolism is dysregulated in sepsis and related conditions, we have shown that T cells are able to control the synthesis and metabolism of BAs, a process which depends on TNF and IFN-γ.
Thus, our work demonstrates the advantage of genome-scale screening with Cas9 and validates NLRX1 as a potential modulator of TNF-α-induced vascular endothelial apoptosis during sepsis.
CONCLUSIONS The levels of plasma BNP and cTnI are associated with the severity of sepsis in pediatric patients, and were positively correlated with CRP and TNF-alpha levels, which provides a novel strategy for the early diagnosis and evaluation of sepsis in pediatric patients.
Sepsis is more common in the elderly.TNF⍺ is recognized as an important mediator in sepsis and Toll-like receptors (TLRs) play an important role in initiating signaling cascades to produce TNF⍺.
Tumor necrosis factor-α (TNFα) is a major cytokine that is highly expressed in many diseased conditions, such as inflammatory diseases, sepsis, and cancer.
<b>Expert opinion</b>: TNFα antagonists may be more immunosuppressive than non-TNF-targeted biologic agents and increase the risk of systemic infections.
Wild type (WT) mice treated with poly(I:C) exhibited altered expression patterns of TNF and IL-12p40 during CASP which were dependent on IFNβ or IFNAR1, suggesting a mechanism for the increased sepsis susceptibility of WT mice.
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.
This work investigated the influence of aqueous ethanol extract of whole plant of SOL and contribution of its main components on inflammation METHODS AND RESULTS: Oral administration of SOL (10 mg/kg) to mice reduced the expression of inflammatory cytokines including IL-6, IL-1β, and TNF-α, in the LPS-induced sepsis mouse model.
We have previously described a model of chronic alcohol ingestion followed by sepsis from cecal ligation and puncture in which alcohol-fed septic mice have higher mortality than water-fed septic mice, associated with altered gut integrity and increased production of TNF and IFNγ by splenic CD4 T cells without alterations in CD8 T cell function.
Although KEGG showed inflammatory bowel disease in the E. coli group, the KEGG pathway analysis showed that these DEGs were mainly involved in the tumor necrosis factor signaling pathway, fructose metabolism, and mannose metabolism in both <i>S. aureus</i>- and <i>E. coli</i>-induced sepsis.
Then, Caco-2 monolayers were utilized to further investigate the protective effect of the EcN supernatant (EcN<sup>sup</sup>) on the barrier dysfunction induced by TNF-<i>α</i> and IFN-<i>γ</i> in vitro; the plasma level of both the cytokines increased significantly during sepsis.
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.
We investigated HRG's role in the LPS/TNF-α-induced barrier dysfunction of endothelial cells in vitro and in vivo and the possible mechanism, to clarify the definitive roles of HRG in sepsis.
lncRNA ITSN1-2 was highly expressed in sepsis patients compared to healthy controls and could differentiate sepsis patients from healthy controls with area under the curve (AUC) 0.777 (95% CI: 0.740-0.813). lncRNA ITSN1-2 expression was positively correlated with APACHE II score, C-reactive protein (CRP), TNF-α, IL-6, and IL-8 levels, but negatively correlated with IL-10 level.