Role of Toll-Like Receptor-4 in Lung Ischemia-Reperfusion Injury

Merry, Heather E.; Phelan, Patrick J.; Doak, Mathew R.; Zhao, Minqing; Hwang, Billanna; Mulligan, Michael S.

doi:10.1016/j.athoracsur.2014.12.062

Cited by 38 publications

(19 citation statements)

References 33 publications

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“…The result enhanced AM production of interferon (IFN)-γ and IL-10, reduced production of TNF-α and IL-1β and promoted lung protection. 32 Notably, those findings from experimental models of lung IRI are consistent with recent human genomic studies of PGD. 11,23 …”

Section: Alveolar Macrophagessupporting

confidence: 83%

Report of the ISHLT Working Group on Primary Lung Graft Dysfunction Part III: Mechanisms: A 2016 Consensus Group Statement of the International Society for Heart and Lung Transplantation

Gelman

Fisher

Huang

et al. 2017

The Journal of Heart and Lung Transplantation

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Section: Alveolar Macrophagessupporting

confidence: 83%

Report of the ISHLT Working Group on Primary Lung Graft Dysfunction Part III: Mechanisms: A 2016 Consensus Group Statement of the International Society for Heart and Lung Transplantation

Gelman

Fisher

Huang

et al. 2017

The Journal of Heart and Lung Transplantation

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“… 15 Currently, it was considered that systemic inflammatory response caused by the extracorporeal circulation and lung ischemia-reperfusion injury can lead to lung injury after extracorporeal circulation cardiac surgery. 16 - 18 Currently, the recognized possible mechanisms are: 1) ischemia-reperfusion injury results in reactive oxygen species and inflammatory molecules (especially cytokines) releasing into the circulation, 19 2) activation of white blood cells, platelets, complements and the blood coagulation system, and the releases of other inflammatory cytokines, which may be secondary to the contact of blood with extracorporeal circulation pipe, 20 and 3) relative insufficient visceral blood perfusion in intraoperative and postoperative can cause intestinal ischemia and increased capillary permeability, and this may lead to intestinal flora ectopicly entering into circulation. The pathophysiological process of DHCA is similar to the lung transplantation after cryopreserved process or the ischemia and reperfusion process of the lung.…”

Section: Discussionmentioning

confidence: 99%

Independent risk factors for hypoxemia after surgery for acute aortic dissection

Wei

Yang²,

Chi

et al. 2015

SMJ

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Objectives:To determine risk factors associated with postoperative hypoxemia after surgery for acute type A aortic dissection.Methods:We retrospectively analyzed the clinical data of 192 patients with acute type A aortic dissection who underwent surgery in Qingdao Municipal Hospital, Medical College of Qingdao University, Qingdao, China between January 2007 and December 2013. Patients were divided into hypoxemia group (n=55) [arterial partial pressure of oxygen (PaO2)/fraction of inspired oxygen (FiO2) ≤200 mm Hg] and non-hypoxemia group (n=137) [PaO2/FiO2 >200 mm Hg]. Perioperative clinical data were analyzed and compared between the 2 groups.Results:The incidence of postoperative hypoxemia after surgery for acute aortic dissection was 28.6% (55/192). Perioperative death occurred in 13 patients (6.8%). Multivariate regression identified body mass index (BMI) >25 kg/m2 (OR=21.929, p=0.000), deep hypothermic circulatory arrest (DHCA) (OR=11.551, p=0.000), preoperative PaO2/FiO2 ≤300 mm Hg (OR=7.830, p=0.000) and blood transfusion >6U in 24 hours postoperatively (OR=12.037, p=0.000) as independent predictors of postoperative hypoxemia for patients undergoing Stanford A aortic dissection surgery.Conclusion:Our study demonstrated that BMI >25 kg/m2, DHCA, preoperative PaO2/FiO2 ≤300 mm Hg, and blood transfusion in 24 hours postoperatively >6U were independent risk factors of the hypoxemia after acute type A aortic dissection aneurysm surgery.

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“…TLR4 has been implicated as a key modulator of lung IR injury [16], and Merry et al . recently utilized siRNA knockdown of TLR4 in rats to demonstrate that TLR4 activation, largely in alveolar macrophages, is important for the initiation of lung IR injury [17]. Phelan et al used an in vitro model to confirm that TLR4 modulates cytokine responses of alveolar macrophages after acute hypoxia-reoxygenation [18].…”

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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Role of Toll-Like Receptor-4 in Lung Ischemia-Reperfusion Injury

Cited by 38 publications

References 33 publications

Report of the ISHLT Working Group on Primary Lung Graft Dysfunction Part III: Mechanisms: A 2016 Consensus Group Statement of the International Society for Heart and Lung Transplantation

Report of the ISHLT Working Group on Primary Lung Graft Dysfunction Part III: Mechanisms: A 2016 Consensus Group Statement of the International Society for Heart and Lung Transplantation

Independent risk factors for hypoxemia after surgery for acute aortic dissection

Mechanisms of lung ischemia-reperfusion injury

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