Functional Roles of Tumor Necrosis Factor-Alpha and Interleukin 1-Beta in Hypoxia and Reoxygenation

Merry, Heather E.; Phelan, Patrick J.; Doaks, Matthew; Zhao, Minqing; Mulligan, Michael S.

doi:10.1016/j.athoracsur.2014.11.042

Cited by 16 publications

(10 citation statements)

References 17 publications

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“…This effect was also evidenced by histopathological analysis. Cytokines are another set of important target genes of NF- κ B, as evidenced by the predominance of TNF- α and IL-1 β in the early stage of inflammation [33]. The release of TNF- α and IL-1 β leads to secondary inflammatory cascades that increase levels of ROS, cytokines, and adhesion molecules, resulting in further damage to lung tissue [34].…”

Section: Discussionmentioning

confidence: 99%

Liver X Receptor Agonist TO901317 Attenuates Paraquat-Induced Acute Lung Injury through Inhibition of NF-κB and JNK/p38 MAPK Signal Pathways

Shen

Wang

et al. 2017

BioMed Research International

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Paraquat (PQ) is a widely used herbicide with extremely high poisoning mortality mostly from acute lung injury (ALI) or progressive pulmonary fibrosis. Toxicity mechanisms remain unclear, but a redox cycling process that generates reactive oxygen species (ROS) is involved, as are inflammation and cell apoptosis. We established an ALI mouse model by intraperitoneal injection of PQ (28 mg/kg) and then investigated the effects of a potent liver X receptor (LXR) agonist, TO901317 (5 or 20 mg/kg), injected intraperitoneally 30 min after PQ administration. Poisoned mice exhibited severe lung tissue lesions and edema, significant neutrophilic (PMNs) infiltration, and release of the proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). PQ administration also decreased activity of antioxidases, including superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferases (GSTs), and increased lipid peroxidation as evaluated by malondialdehyde (MDA) levels. PQ exposure induced upregulation of the proapoptotic gene Bax and downregulation of the antiapoptotic gene Bcl-2, leading to marked cell apoptosis in the lung tissues. TO901317 treatment reversed all these effects through inhibition of PQ-induced nuclear factor kappa B (NF-κB) and JNK/p38 mitogen-activated protein kinase (MAPK) activation. The LXR agonist TO901317 had potent antioxidant, anti-inflammatory, and antiapoptotic effects against PQ-induced ALI.

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Section: Discussionmentioning

confidence: 99%

Liver X Receptor Agonist TO901317 Attenuates Paraquat-Induced Acute Lung Injury through Inhibition of NF-κB and JNK/p38 MAPK Signal Pathways

Shen

Wang

et al. 2017

BioMed Research International

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“…Induced NO contributes to ongoing oxidative damage to trabecular tissues, because RNS leads to the direct activation of macrophages and their production of TNFa and IL-1b. 173 TNFa, a potent proinflammatory cytokine, orchestrates the inflammatory response in many immune-mediated and autoimmune diseases. Upregulated TNFa is also implicated in other neurodegenerative diseases like Alzheimer and Parkinson.…”

Section: Activation Of Glial Cellsmentioning

confidence: 99%

Definition, Classification, and Pathophysiology of Canine Glaucoma

Pizzirani

2015

Veterinary Clinics of North America: Small Animal Practice

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“…Phelan et al used an in vitro model to confirm that TLR4 modulates cytokine responses of alveolar macrophages after acute hypoxia-reoxygenation [18]. A third study by this group demonstrated that TNF-α and IL-1β, secreted by alveolar macrophages, prime and amplify the response of endothelial and epithelial cells through parallel pathways after exposure to hypoxia-reoxygenation [19]. Finally, although IR injury is considered a sterile inflammatory condition, an interesting study by Prakash et al .…”

Section: Innate Immune Responsesmentioning

confidence: 99%

Mechanisms of lung ischemia-reperfusion injury

Laubach

Sharma²

2016

Current Opinion in Organ Transplantation

192

191

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Purpose of review Lungs are extremely susceptible to injury, and despite advances in surgical management and immunosuppression, outcomes for lung transplantation are the worst of any solid organ transplant. The success of lung transplantation is limited by high rates of primary graft dysfunction (PGD) due to ischemia-reperfusion (IR) injury characterized by robust inflammation, alveolar damage and vascular permeability. This review will summarize major mechanisms of lung IR injury with a focus on the most recent findings in this area. Recent findings Over the past 18 months numerous studies have described strategies to limit lung IR injury in experimental settings, which often reveal mechanistic insight. Many of these strategies involved the use of various anti-oxidants, anti-inflammatory agents, mesenchymal stem cells, and ventilation with gaseous molecules. Further advancements have been achieved in understanding mechanisms of innate immune cell activation, neutrophil infiltration, endothelial barrier dysfunction, and oxidative stress responses. Summary Methods for prevention of PGD after lung transplant are urgently needed, and understanding mechanisms of IR injury is critical for the development of novel and effective therapeutic approaches. In doing so, both acute and chronic outcomes of lung transplant recipients will be significantly improved.

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Functional Roles of Tumor Necrosis Factor-Alpha and Interleukin 1-Beta in Hypoxia and Reoxygenation

Cited by 16 publications

References 17 publications

Liver X Receptor Agonist TO901317 Attenuates Paraquat-Induced Acute Lung Injury through Inhibition of NF-κB and JNK/p38 MAPK Signal Pathways

Liver X Receptor Agonist TO901317 Attenuates Paraquat-Induced Acute Lung Injury through Inhibition of NF-κB and JNK/p38 MAPK Signal Pathways

Definition, Classification, and Pathophysiology of Canine Glaucoma

Mechanisms of lung ischemia-reperfusion injury

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