Mechanisms of bacterial lipopolysaccharide-induced endothelial apoptosis.

  title={Mechanisms of bacterial lipopolysaccharide-induced endothelial apoptosis.},
  author={Douglas D. Bannerman and Simeon E. Goldblum},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  volume={284 6},
  • D. Bannerman, S. Goldblum
  • Published 1 June 2003
  • Biology, Medicine
  • American journal of physiology. Lung cellular and molecular physiology
Gram-negative bacterial sepsis remains a common, life-threatening event. The prognosis for patients who develop sepsis-related complications, including the development of acute respiratory distress syndrome (ARDS), remains poor. A common finding among patients and experimental animals with sepsis and ARDS is endothelial injury and/or dysfunction. A component of the outer membrane of gram-negative bacteria, lipopolysaccharide (LPS) or endotoxin, has been implicated in the pathogenesis of much of… 

Figures from this paper

Emerging role of Lipopolysaccharide binding protein in sepsis-induced acute kidney injury

  • A. StasiA. Intini G. Castellano
  • Biology, Medicine
    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
  • 2017
Recent findings regarding the emerging role of LBP in mediating sepsis-induced AKI, and the possible beneficial effects resulting from the removal of this endogenous adaptor protein, will be discussed in this review.

Human anti-microbial cathelicidin peptide LL-37 suppresses the LPS-induced apoptosis of endothelial cells.

LL-37 could suppress the LPS-induced apoptosis of endothelial cells, thereby attenuating lethal sepsis/endotoxin shock, and this study investigated the effects of LL-37 on the L PS-induced endothelial cell apoptosis in vitro and in vivo.

The Intrinsic Apoptotic Pathway Is Required for Lipopolysaccharide-Induced Lung Endothelial Cell Death1

It is concluded that LPS and cycloheximide-induced death in HmVECs requires the intrinsic cell death pathway, but not the generation of reactive oxygen species.

Leukocyte apoptosis and its significance in sepsis and shock

As inhibiting Fas‐FasL signaling, caspase inhibition, and/or the overexpression of downstream antiapoptotic molecules improve survival of septic mice, it not only demonstrates the pathological significance of this process but points to novel targets for the treatment of sepsis.

C1 inhibitor prevents Gram-negative bacterial lipopolysaccharide-induced vascular permeability.

It is reported that C1INH blocked the LPS-induced increase in transendothelial flux through an endothelial monolayer, and inhibited L PS-induced endothelial cell apoptosis as demonstrated by suppression of DNA fragmentation and annexin V expression.

Lipopolysaccharide Induces Human Pulmonary Micro-Vascular Endothelial Apoptosis via the YAP Signaling Pathway

It is demonstrated that activation of the YAP/P73/(BAX and BCL-2)/caspase-3 signaling pathway played a critical role in LPS-induced HPMEC apoptosis and inhibition of YAP by small interfering RNA might be a potential therapeutic strategy for lung injury under sepsis.

Response to Endotoxin Endothelial Junction Protein p120-Catenin in Innate Immune Function of the Adherens

A novel innate immune function of endothelial p120 is uncovered in downregulating the lung inflammatory response to endotoxin through the suppression of TLR4 signaling.

Innate Immune Function of the Adherens Junction Protein p120-Catenin in Endothelial Response to Endotoxin

These studies have uncovered a novel innate immune function of endothelial p120 in downregulating the lung inflammatory response to endotoxin through the suppression of TLR4 signaling.

Malaria and bacterial sepsis: Similar mechanisms of endothelial apoptosis and its prevention in vitro*

These in vitro results show how neutrophils can contribute to endothelial damage in malaria and in sepsis, both by their secretory products and by binding to intercellular adhesion molecule-1 on endothelial cells.



Lipopolysaccharide Mediates Endothelial Apoptosis by a FADD-dependent Pathway*

It is demonstrated that LPS mediates endothelial apoptosis by a FADD-dependent pathway that binds to certain members of the tumor necrosis factor receptor family, namely TNFR1, Fas, and DR3.

Divergence of Bacterial Lipopolysaccharide Pro-apoptotic Signaling Downstream of IRAK-1*

Using a variety of dominant negative constructs, a role is identified for MyD88 and interleukin-1 receptor-associated kinase-1 (IRAK-1) in mediating LPS pro-apoptotic signaling in human endothelial cells and it is demonstrated that LPS-induced endothelial NF-κB activation and apoptosis occur independent of one another.

Endotoxin-Mediated Endothelial Cell Injury and Activation: Role of Soluble CD14

It is shown that serum was required for LPS-mediated cytotoxicity for bovine brain microvessel, pulmonary, and aortic ECs and that anti-human CD14 antibodies completely blocked L PS- mediated cytot toxicity for ECs in the presence of human serum, suggesting that serum soluble CD14 represents a naturally occurring agonist for EC responses to LPS.

Lipopolysaccharide induces the antiapoptotic molecules, A1 and A20, in microvascular endothelial cells.

LPS directly induces expression of the cytoprotective proteins, A1 and A20, via a CD14-dependent pathway requiring activation of NF-kappaB, and it is demonstrated that both these molecules are induced in microvascular endothelial cells by LPS.

A Constitutive Cytoprotective Pathway Protects Endothelial Cells from Lipopolysaccharide-induced Apoptosis*

Reduction of FLIP expression with antisense oligonucleotides sensitized endothelial cells to LPS killing, demonstrating a definitive role for FLIP in the protection of endothelium cells from LPS-induced apoptosis.

Acute inflammation and microthrombosis induced by endotoxin, interleukin-1, and tumor necrosis factor and their implication in gram-negative infection.

Both the inflammatory and the thrombotic phenomena induced by endotoxin are mediated by the local generation of cytokines, and neutrophils are the primary effector cells in this process.

Receptor-dependent mechanisms of cell stimulation by bacterial endotoxin.

How LBP enables LPS binding to CD14 and how complexes of LPS and soluble or GPI-anchored CD14 participate in cell activation are discussed, and the evidence supporting a model for a functional LPS receptor of myeloid cells, which is multimeric, is reviewed.

Lipopolysaccharide-Induced Apoptosis of Endothelial Cells and Its Inhibition by Vascular Endothelial Growth Factor

It is observed that pretreatment with vascular endothelial growth factor (VEGF), a known cell survival factor, blocked LPS-induced apoptosis in endothelial cells and suggested that VEGF inhibits L PS-induced endothelial apoptosis by blocking pathways that lead to caspase activation.

Protection from lethal apoptosis in lipopolysaccharide-induced acute lung injury in mice by a caspase inhibitor.

Tumor necrosis factor-alpha and lipopolysaccharide induce apoptotic cell death in bovine glomerular endothelial cells.

Both bacterial LPS and TNF-alpha potently induced apoptotic cell death in glomerular endothelial cells, and direct endotoxin-induced apoptosis may be relevant in the progression of acute renal failure, which is a frequent complication of gram-negative sepsis.