Long pentraxin 3 in pulmonary infection and acute lung injury

2007 ◽  
Vol 292 (5) ◽  
pp. L1039-L1049 ◽  
Author(s):  
Xiaolin He ◽  
Bing Han ◽  
Mingyao Liu
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Infection ◽  
Ischemia Reperfusion ◽  
High Volume ◽  
Pentraxin 3 ◽  
Experimental Conditions ◽  
Novel Therapeutic Strategies ◽  
Intestinal Ischemia Reperfusion ◽  
Severe Lung

Long pentraxin 3 (PTX3) is a newly discovered acute phase protein produced at the sites of infection and inflammation by tissue cells, macrophages, monocytes, and dendritic cells. PTX3 plays an important role in preventing infection of certain fungi, bacteria, and viruses in the lung. Recombinant PTX3 has been proposed as a potential antifungal molecule for therapy. However, under certain experimental conditions, such as intestinal ischemia-reperfusion, high volume mechanical ventilation, or severe bacterial infection, increased expression of PTX3 is associated with more severe lung injury. Therefore, it is necessary to further explore the sources of PTX3 in the lung and the regulatory mechanisms of its expression. It is also essential to further determine how PTX3 binds to pathogens, complement, and apoptotic cells, and to determine whether PTX3 has a specific receptor in targeted cells. These studies will provide insight into the pathological processes of pulmonary infection and acute lung injury and provide potential novel therapeutic strategies to control pulmonary infections without severe lung injury.

scholarly journals Corrigendum to: Acute Lung Injury in A Rat Model Of Intestinal Ischemia-Reperfusion: The Potential Time Depended Role Of Phospholipases

2021 ◽  
Vol 263 ◽  
pp. 291
Author(s):  
Georgia Kostopanagiotou ◽  
Efthimios Avgerinos ◽  
Konstantinos Kostopanagiotou ◽  
Nikolaos Arkadopoulos ◽  
Ioanna Andreadou ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Rat Model ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

scholarly journals Nrf2 Activation Induced by Sirt1 Ameliorates Acute Lung Injury After Intestinal Ischemia/Reperfusion Through NOX4-Mediated Gene Regulation

2018 ◽  
Vol 46 (2) ◽  
pp. 781-792 ◽  
Author(s):  
DongDong Chai ◽  
Lei Zhang ◽  
SiWei Xi ◽  
YanYong Cheng ◽  
Hong Jiang ◽  
...  
Keyword(s):  
Gene Regulation ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Vegf Expression ◽  
Intestinal Ischemia Reperfusion ◽  
Cd31 Expression

Background/Aims: Nuclear erythroid 2-related factor-2 (Nrf2) is a major stress-response transcription factor that has been implicated in regulating ischemic angiogenesis. We investigated the effects of Nrf2 in regulating revascularization and modulating acute lung injury. Methods: The expression of Nrf2 and sirtuin1 (Sirt1) was assessed in lung tissue by western blotting and immunofluorescence staining after intestinal ischemia/reperfusion (IIR) in Nrf2–/– and wild-type (WT) mice. The involvement of Nrf2 in angiogenesis, cell viability, and migration was investigated in human pulmonary microvascular endothelial cells (PMVECs). Additionally, the influence of Nrf2 expression on NOX pathway activation was measured in PMVECs after oxygen–glucose deprivation/reoxygenation. Results: We found activation and nuclear accumulation of Nrf2 in lung tissue after IIR. Compared to IIR in WT mice, IIR in Nrf2–/– mice significantly enhanced leukocyte infiltration and collagen deposit, and inhibited endothelial cell marker CD31 expression. Nrf2 upregulation and translocation into the nucleus stimulated by Sirt1 overexpression exhibited remission of histopathologic changes and enhanced CD31 expression. Nrf2 knockdown repressed non-phagocytic cell oxidase 4 (NOX4), hypoxia-inducible factor (HIF-1α) and vascular endothelial growth factor (VEGF) expression after IIR. Nrf2 upregulation by Sirt1 enhances NOX4, HIF-1α and VEGF expression after IIR in WT mice. Furthermore, Nrf2 knockdown suppressed cell viability, capillary tube formation and cell migration in PMVECs after oxygen–glucose deprivation/reoxygenation and also inhibited NOX4, HIF-1 and VEGF expression. Moreover, NOX4 knockdown in PMVECs decreased the levels of VEGF, HIF-1α and angiogenesis. Conclusion: Nrf2 stimulation by Sirt1 plays an important role in sustaining angiogenic potential through NOX4-mediated gene regulation.

scholarly journals Role of iRhom2 in intestinal ischemia-reperfusion-mediated acute lung injury

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Jee Hyun Kim ◽  
Jihye Kim ◽  
Jaeyoung Chun ◽  
Changhyun Lee ◽  
Jong Pil Im ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

High-volume ventilation induces pentraxin 3 expression in multiple acute lung injury models in rats

2007 ◽  
Vol 292 (1) ◽  
pp. L144-L153 ◽  
Author(s):  
Daisuke Okutani ◽  
Bing Han ◽  
Marco Mura ◽  
Thomas K. Waddell ◽  
Shaf Keshavjee ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
High Volume ◽  
Pentraxin 3 ◽  
Sprague Dawley ◽  
Ventilator Induced Lung Injury ◽  
Sprague Dawley Rats ◽  
Volume Ventilation ◽  
Highly Correlated ◽  
Injury Models

Pentraxin 3 (PTX3) is an acute-phase protein, which can be produced by a variety of tissue cells at the site of infection or inflammation. It plays an important role in innate immunity in the lung and in mediating acute lung injury. The aim of this study was to determine the effect of mechanical ventilation on PTX3 expression in multiple lung injury models. Male Sprague-Dawley rats were challenged with intravenous injection of lipopolysaccharide (LPS) or hemorrhage followed by resuscitation (HS). The animals were then subjected to either relatively higher (12 ml/kg) or lower (6 ml/kg, positive end-expiratory pressure of 5 cmH2O) volume ventilation for 4 h. High-volume ventilation significantly enhanced PTX3 expression in the lung, either alone or in combination with LPS or hemorrhage. A significant increase of PTX3 immunohistochemistry staining in the lung was seen in all injury groups. The PTX3 expression was highly correlated with the severity of lung injury determined by blood gas, lung elastance, and wet-to-dry ratio. To determine the effects of HS, LPS, or injurious ventilation (25 ml/kg) alone on PTX3 expression, another group of rats was studied. Injurious ventilation significantly damaged the lung and increased PTX3 expression. A local expression of PTX3 induced by high-volume ventilation, either alone or in combination with other pathological conditions, suggests that it may be an important mediator in ventilator-induced lung injury.

scholarly journals Nrf2 inhibits ferroptosis and protects against acute lung injury due to intestinal ischemia reperfusion via regulating SLC7A11 and HO-1

Aging ◽  
2020 ◽  
Vol 12 (13) ◽  
pp. 12943-12959 ◽  
Author(s):  
Hui Dong ◽  
Zhuanzhuan Qiang ◽  
Dongdong Chai ◽  
Jiali Peng ◽  
Yangyang Xia ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

scholarly journals Author Correction: Role of iRhom2 in intestinal ischemia-reperfusion-mediated acute lung injury

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Jee Hyun Kim ◽  
Jihye Kim ◽  
Jaeyoung Chun ◽  
Changhyun Lee ◽  
Jong Pil Im ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

scholarly journals Nrf2 and STAT3 Alleviates Ferroptosis-Mediated IIR-ALI by Regulating SLC7A11

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Zhuanzhuan Qiang ◽  
Hui Dong ◽  
Yangyang Xia ◽  
Dongdong Chai ◽  
Rong Hu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Warning Signal ◽  
Antioxidant Stress ◽  
Intestinal Ischemia Reperfusion ◽  
Transcription 3

Acute lung injury (ALI) has gained increased attention in the field of critical illness research and is associated with a fatality rate of approximately 50%. Nuclear factor erythroid 2-related factor2 (Nrf2) is a key regulator of intracellular oxidation homeostasis and also functions as an antioxidant. It has been reported that Nrf2 associated antioxidant stress is closely related to ferroptosis inhibition. Signal transducer and activator of transcription 3 (STAT3) is activated into phosphorylated STAT3 (pSTAT3) in response to tissue damage and serves as a warning signal to enhance the inflammatory response. In this study, an intestinal ischemia/reperfusion-induced acute lung injury (IIR-ALI) model was established in C57BL/6 mice to investigate the role of Nrf2 in regulating IIR-ALI-associated ferroptosis. Compared with those in the IIR-ALI group, the injection of Fe (15 mg/kg) or ferrostatin-1 (5 mg/kg) (ferroptosis promoter and inhibitor, respectively) via the tail vein could aggravate or alleviate lung injury and pulmonary edema, respectively. Nrf2 was increased in IIR-ALI and promoted the phosphorylation of STAT3 to amplify downstream signals. An in vitro oxygen-glucose deprivation and reoxygenation (OGD-R) model was established in MLE12 cells to imitate the ischemia/reperfusion condition. The cells were transfected with lentiviruses to increase or downregulate the levels of STAT3. We found that Nrf2 and STAT3 played key roles in ferroptosis by regulating SLC7A11, which improved the pathological processes associated with ALI.

Sign in / Sign up

Export Citation Format

Share Document