Burn-activated neutrophils and tumor necrosis factor-α alter endothelial cell actin cytoskeleton and enhance monolayer permeability

Wright, Keith; Nwariaku, Fiemu E.; Halaihel, Nabil; Schulman, Carl I.; Yin, Helen L.; Turnage, Richard H.

doi:10.1067/msy.2000.108215

Cited by 17 publications

(6 citation statements)

References 17 publications

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“…On the other hand, a hallmark of burn-induced pulmonary injury is accumulation of neutrophils within the lung (20). Exposure of endothelial cells to neutrophils from burned patients results in rounding and shrinking of the cells and subsequent hyperpermeability across the monolayer (29). The neutrophils themselves undergo dramatic changes after thermal injury.…”

Section: Discussionmentioning

confidence: 99%

Myosin light chain phosphorylation and pulmonary endothelial cell hyperpermeability in burns

Tinsley¹,

Teasdale²,

Yuan³

2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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Major cutaneous burns result in not only localized tissue damage but broad systemic inflammation causing organ system damage distal to the burn site. It is well recognized that many problems result from the release of inflammatory mediators that target vascular endothelial cells, causing organ dysfunction. The pulmonary microvessels are particularly susceptible to functional abnormalities as a direct consequence of exposure to burn-induced inflammatory mediators. Traditional therapeutic intervention is quite often ineffective in treating burn patients suffering from systemic problems. A possible explanation for this ineffectiveness may be that because so many mediators are released, supposedly activating numerous signaling cascades that interact with each other, targeting of upstream factors in these cascades on an individual basis becomes futile. Therefore, if an end-point effector responsible for endothelial dysfunction following burn injury could be identified, it may present a target for intervention. In this study, we identified phosphorylation of myosin light chain (MLC) as a required element of burn plasma-induced hyperpermeability across rat lung microvascular endothelial cell monolayers. In addition, pharmacological inhibition of myosin light chain kinase (MLCK) and Rho kinase as well as transfection of MLCK-inhibiting peptide blocked actin stress fiber formation and MLC phosphorylation in response to burn plasma. The results suggest that blocking MLC phosphorylation may provide therapeutic intervention in burn patients with the goal of alleviating systemic inflammation-induced endothelial dysfunction.

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Section: Discussionmentioning

confidence: 99%

Myosin light chain phosphorylation and pulmonary endothelial cell hyperpermeability in burns

Tinsley¹,

Teasdale²,

Yuan³

2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…TNF-a at 100 ng/ml was then added followed by another incubation of 6 h. Growth medium was removed and cell monolayer was washed with Hank's balanced salt solution (HBSS) containing 20 mM HEPES (HBSS/HEPES) three times. Then 100 Al of media that containing Evans Blue dyebound albumin (EBD-BSA; prepared by the method of Wright et al [21]) was added to the upper compartment. 600 Al of HBSS/HEPES buffer was kept in the lower compartment.…”

Section: Measurement Of Huvec Monolayer Permeability By Evans Blue Dymentioning

confidence: 99%

Aqueous extract of Salvia miltiorrhiza attenuates increased endothelial permeability induced by tumor necrosis factor-α

Ding

Zhao

et al. 2005

International Immunopharmacology

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“…Cytokines that are liberated from the intestine during ischaemia‐reperfusion can directly affect the intestinal barrier. TNF‐α induces the permeability of intestinal epithelial [46] and endothelial cells [47] by altering the actin cytoskeleton [48]. Blockade of TNF‐α significantly reduces the extent of bacterial translocation [49].…”

Section: The Role Of the Intestine In The Development Of Sirs/mods Inmentioning

confidence: 99%

The role of the intestine in the pathophysiology and management of severe acute pancreatitis

Flint

Windsor

2003

HPB

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BackgroundThe outcome of severe acute pancreatitis has scarcely improved in 10 years. Further impact will require new paradigms in pathophysiology and treatment. There is accumulating evidence to support the concept that the intestine has a key role in the pathophysiology of severe acute pancreatitis which goes beyond the notion of secondary pancreatic infection. Intestinal ischaemia and reperfusion and barrier failure are implicated in the development of multiple organ failure. DiscussionConventional management of severe acute pancreatitis has tended to ignore the intestine. More recent attempts to rectify this problem have included 1) resuscitation aimed at restoring intestinal blood¯ow through the use of appropriate¯uids and splanchnic-sparing vasoconstrictors or inotropes; 2) enteral nutrition to help maintain the integrity of the intestinal barrier;3) selective gut decontamination and prophylactic antibiotics to reduce bacterial translocation and secondary infection.Novel therapies are being developed to limit intestinal injury, and these include antioxidants and anti-cytokine agents. This paper focuses on the role of the intestine in the pathogenesis of severe acute pancreatitis and reviews the implications for management.

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Burn-activated neutrophils and tumor necrosis factor-α alter endothelial cell actin cytoskeleton and enhance monolayer permeability

Cited by 17 publications

References 17 publications

Myosin light chain phosphorylation and pulmonary endothelial cell hyperpermeability in burns

Myosin light chain phosphorylation and pulmonary endothelial cell hyperpermeability in burns

Aqueous extract of Salvia miltiorrhiza attenuates increased endothelial permeability induced by tumor necrosis factor-α

The role of the intestine in the pathophysiology and management of severe acute pancreatitis

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