Tumor necrosis factor alpha-induced pulmonary vascular endothelial injury

Goldblum, Simeon E.; Hennig, Bernhard; Jay, M. A.; Yoneda, K; McClain, Craig J.

doi:10.1128/iai.57.4.1218-1226.1989

Cited by 126 publications

(43 citation statements)

References 30 publications

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“…When released in the lung, TNFa exerts devastating effects causing rapid and diffuse tissue i n j~r y .~'~-'~ Some animal models of ARDS have provided evidence that TNFa can cause in pulmonary edema and transudation of plasma protein due to increased vascular permeability. 18,19 TNFa was elevated in rats with experimentally induced acute alveolitis and ARDS.m, 21 We confirmed in this study that the alveolar macrophages were major sources of not only TNFa, but also IL-lp. Piguet et a/.…”

Section: Discussionsupporting

confidence: 67%

Co‐expression of TNFα and IL‐1β in human acute pulmonary fibrotic diseases: An immunohistochemical analysis

Pan

Ohtani

Yamauchi

et al. 1996

Pathology International

107

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To clarify the involvement of TNF alpha and IL-1 beta in the initiation of fibrotic lung diseases, their localization was examined by immunohistochemistry. Fibrotic lung diseases observed were classified into acute and old pulmonary fibrotic changes. The acute fibrotic changes included adult respiratory distress syndrome, acute interstitial pneumonia and idiopathic pulmonary fibrosis with acute exacerbation. Acute pulmonary fibrotic changes histopathologically corresponded to a mixture of the exudative and proliferative phases of diffuse alveolar damage. Both TNF alpha and IL-1 beta were positive in the alveolar macrophages and proliferating type II pneumocytes in acute fibrotic changes. In contrast, positive cells for TNF alpha and IL-1 beta were sparse in the areas of old fibrotic change and in the normal tissue. These findings suggest that TNF alpha and IL-1 beta play an important role in the initiation of pulmonary fibrotic responses and in the architectural remodeling, irrespective of the etiology of fibrotic lung diseases.

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Section: Discussionsupporting

confidence: 67%

Co‐expression of TNFα and IL‐1β in human acute pulmonary fibrotic diseases: An immunohistochemical analysis

Pan

Ohtani

Yamauchi

et al. 1996

Pathology International

107

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“…A prime candidate as a mediator for this effect is TNF, which is released in to the circulation soon after LPS injection (Guo et al 2004). TNF is known to increase permeability of endothelial cells, although this is generally a delayed response (Goldblum et al 1989;Goldblum and Sun 1990). McKenzie and Ridley (2007) showed that the effect of TNF (10-100 ng/mL) on the permeability of HUVEC monolayers was significant 8 h after its addition, and peaked at 24 h. Here, we tested the effect of TNF on the permeability of human glomerular endothelial cells (GEnCs) and mouse primary culture renal endothelial cells (REnCs), which are mainly a mixture of glomerular and peritubular endothelial cells (Wu et al 2009).…”

Section: Barrier Dysfunction Is Induced By Lps In Mice and By Tnf In mentioning

confidence: 99%

TNF causes changes in glomerular endothelial permeability and morphology through a Rho and myosin light chain kinase-dependent mechanism

Hack

et al. 2015

Physiol Rep

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A key function of the endothelium is to serve as a regulated barrier between tissue compartments. We have previously shown that tumor necrosis factor (TNF) plays a crucial role in lipopolysaccharide (LPS)‐induced acute kidney injury, in part by causing injury to the renal endothelium through its receptor TNFR1. Here, we report that TNF increased permeability to albumin in primary culture mouse renal endothelial cells, as well as human glomerular endothelial cells. This process occurred in association with changes in the actin cytoskeleton and was associated with gaps between previously confluent cells in culture and decreases in the tight junction protein occludin. This process was dependent on myosin light chain activation, as seen by its prevention with Rho‐associated kinase and myosin light chain kinase (MLCK) inhibitors. Surprisingly, permeability was not blocked by inhibition of apoptosis with caspase inhibitors. Additionally, we found that the renal glycocalyx, which plays an important role in barrier function, was also degraded by TNF in a Rho and MLCK dependent fashion. TNF treatment caused a decrease in the size of endothelial fenestrae, dependent on Rho and MLCK, although the relevance of this to changes in permeability is uncertain. In summary, TNF‐induced barrier dysfunction in renal endothelial cells is crucially dependent upon the Rho/MLCK signaling pathway.

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“…TNF can trigger endothelial cell activation and barrier dysfunction, which are both implicated in the pathogenesis of pulmonary edema 93 . In 1989, Goldblum et al observed that human recombinant TNF could provoke acute pulmonary vascular endothelial injury and increase pulmonary vascular permeability in vivo as well as in vitro 94 . In another study, TNF is shown to increase the permeability of endothelial cell monolayers to macromolecules and lower molecular weight solutes by a mechanism involving a pertussis toxin-sensitive regulatory G protein 95 .…”

Section: Effects Of Tnf On Permeability Of Epithelialendothelial Barriermentioning

confidence: 99%

The dual role of TNF in pulmonary edema

Yang¹,

Hamacher²,

Gorshkov³

et al. 2010

Journal of Cardiovascular Disease Research

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—Pulmonary edema, a major manifestation of left ventricular heart failure, renal insufficiency, shock, diffuse alveolar damage and lung hypersensitivity states, is a significant medical problem worldwide and can be life-threatening. The proinflammatory cytokine tumor necrosis factor (TNF) has been shown to contribute to the pathogenesis and development of pulmonary edema. However, some recent studies have demonstrated surprisingly that TNF can also promote alveolar fluid reabsorption in vivo and in vitro. This protective effect of the cytokine is mediated by the lectin-like domain of the cytokine, which is spatially distinct from the TNF receptor binding sites. The TIP peptide, a synthetic mimic of the lectin-like domain of TNF, can significantly increase alveolar fluid clearance and improve lung compliance in pulmonary edema models. In this review, we will discuss the dual role of TNF in pulmonary edema.Abbreviations:—tumor necrosis factor (TNF); acute lung injury (ALI); acute respiratory distress syndrome (ARDS); positive end-expiratory pressure (PEEP);epithelial sodium channel (ENaC);neural precursor cell-expressed developmentally downregulated (gene 4) protein (Nedd4-2);serum and glucocorticoid dependent kinase (Sgk-1);insulin-like growth factor 1 (IGF-1);Protein Kinase C (PKC);reactive oxygen species (ROS);myosin light chain (MLC);pneumolysin (PLY);listeriolysin (LLO);interleukin (IL);bronchoalveolar lavage fluids (BALF);Bacillus Calmette-Guerin (BCG);TNF receptor type 1 (TNFR1); TNF receptor type 2 (TNF-R2);

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Tumor necrosis factor alpha-induced pulmonary vascular endothelial injury

Cited by 126 publications

References 30 publications

Co‐expression of TNFα and IL‐1β in human acute pulmonary fibrotic diseases: An immunohistochemical analysis

Co‐expression of TNFα and IL‐1β in human acute pulmonary fibrotic diseases: An immunohistochemical analysis

TNF causes changes in glomerular endothelial permeability and morphology through a Rho and myosin light chain kinase-dependent mechanism

The dual role of TNF in pulmonary edema

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