Treatment of experimental sepsis-induced immunoparalysis with TNF
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Cardiac steroid ouabain transcriptionally increases human leukocyte antigen DR expression on monocytes
2021, SteroidsCitation Excerpt :With the exception of these cytokines-based drugs, few small molecules for the treatment of immunoparalysis has been reported. As a matter of fact, small-molecule drug has relatively poor immunoreactivity, extended half-life, and high penetration efficiency across blood–brain barrier when compared with protein drugs [19,20]. Therefore, identification of small-molecule drug that can modulate HLA-DR expression represents a promising trend in the therapy of sepsis-induced immunoparalysis.
The effect of Indomethacin and Betamethasone on the cytokine response of human neonatal mononuclear cells to gram-positive bacteria
2015, CytokineCitation Excerpt :Studies in animal models show that TNF plays a critical role in the host defense against bacteria. The pro-inflammatory cytokine is not only required by the innate immune system to initially fight off infections, but also helps resolving the inflammatory response by an ensuing down-regulation of pro-inflammatory cytokines [21,22]. The fact that the inhibition of TNF by TNF antagonists in patients with inflammatory diseases increases the risk of opportunistic infections with a variety of pathogens [23] underlines the importance of this cytokine in the host defense against bacteria and other pathogens.
Emerging Therapeutic Targets of Sepsis-Associated Acute Kidney Injury
2015, Seminars in NephrologyCitation Excerpt :Trials for these agents are in various stages (Table 2). Another novel approach has been based on the finding that late sepsis-related deaths often appear to be associated with evidence of immune suppression and dysfunction.10,136 Thus, patients who survive the initial proinflammatory stage may enter an anti-inflammatory phase with variable degrees of immunoparalysis.
Sepsis, apoptosis and complement
2008, Biochemical PharmacologyCitation Excerpt :It should also be noted that approximately 50% of humans with sepsis have gram positive bacterial pneumonia [1–3]. While lipopolysaccharide (LPS) has been speculated to cause harmful outcomes, there is other evidence (in TLR4−/−, CD14−/−, and LPS-binding protein−/− mice) suggesting that, at least in the setting of CLP, LPS may not be a major determinant in the adverse outcomes [19–21]. All three pathways of complement activation converge to generate the “C3 convertase”, which cleaves C3 into a small (C3a) and a large (C3b) fragmentation product (Fig. 1).
Advances in sepsis research derived from animal models
2007, International Journal of Medical MicrobiologyPerinatal gram‐positive bacteria exposure elicits distinct cytokine responses in vitro
2021, International Journal of Molecular Sciences