Modulation of monocyte chemoattractant protein-1 expression by ischaemic preconditioning in a lung autotransplant model

Simón, Carlos; Vara, Elena; Garutti, Ignacio; González-Casaurrán, Guillermo; Azcárate, Leire; Isea, Jesús; Huerta, Luis; González-Aragoneses, Federico

doi:10.1093/ejcts/ezr049

Cited by 8 publications

(6 citation statements)

References 21 publications

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“…2,20,21 Besides reactive oxygen and nitrogen species, massive production of pro-inflammatory cytokines 1,4,5 and reduced expression of growth factors 6 plays a central role in mediating inflammation in ARDS. 1,5 For instance, IL-1β, a potent pro-inflammatory cytokine, is centrally involved in the mechanism of lung injury and regulates microvascular endothelial permeability. 47 Here, we observed that Cr supplementation reduced I/R-induced high plasma levels of IL-1β, which was followed by reduced pulmonary perivascular edema.…”

Section: Figurementioning

confidence: 99%

Creatine supplementation attenuates pulmonary and systemic effects of lung ischemia and reperfusion injury

Almeida

Oliveira-Júnior

Souza

et al. 2016

The Journal of Heart and Lung Transplantation

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Section: Figurementioning

confidence: 99%

Creatine supplementation attenuates pulmonary and systemic effects of lung ischemia and reperfusion injury

Almeida

Oliveira-Júnior

Souza

et al. 2016

The Journal of Heart and Lung Transplantation

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“…Ischaemic conditioning has a myriad of effects on the inflammatory response to IR, it reduces the expression of inflammatory cytokines such as TNF-α, IL1b, IL6, CCL2; reduces leucocyte recruitment and extravasation by downregulating ICAM [ 107 , 111 , 113 ]. The reduction in neutrophil chemotaxis and activity also reduces of the production of ROS, as seen by a reduction in MDA and lipid hydroperoxides (LPO) production [ 27 ]. In addition, ischaemic conditioning also reduces mediators of apoptosis, including BAX, Caspase, cytochrome C and Fas ligand [ 108 , 112 ].…”

Section: Novel Therapies For Ischaemia–reperfusion Injurymentioning

confidence: 99%

“…IRI is often characterised by rapid accumulation of ROS soon after reperfusion, with increased activities of ROSgenerating enzymes such as NADPH oxidase, xanthine oxidase and myeloperoxidase [8,17,22,23]. Reduction in anti-oxidative capacity [15,24] and the occurrence of oxidative stress [24][25][26][27] are also observed. NADPH oxidase activity seems to play a significant role in the pathophysiology of IRI, as NADPH oxidase knockout animal demonstrates significantly blunted oxidative stress and inflammatory response to IRI.…”

Section: Oxidative and Nitrosative Stressmentioning

confidence: 99%

Review 2: Primary graft dysfunction after lung transplant—pathophysiology, clinical considerations and therapeutic targets

et al. 2020

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Primary graft dysfunction (PGD) is one of the most common complications in the early postoperative period and is the most common cause of death in the first postoperative month. The underlying pathophysiology is thought to be the ischaemia–reperfusion injury that occurs during the storage and reperfusion of the lung engraftment; this triggers a cascade of pathological changes, which result in pulmonary vascular dysfunction and loss of the normal alveolar architecture. There are a number of surgical and anaesthetic factors which may be related to the development of PGD. To date, although treatment options for PGD are limited, there are several promising experimental therapeutic targets. In this review, we will discuss the pathophysiology, clinical management and potential therapeutic targets of PGD.

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“…When the antioxidant defense capabilities of the lung, for example, are overburdened and unable to cope with the increase in ROS, deviations in cellular metabolic function and redox signaling occur. Oxidative stress due to ROS causes proin ammatory cytokine release and enhanced transcription of numerous genes resulting in in ammation, cell injury, and neutrophil recruitment and activation in the lung after ischemic reperfusion (IR) and reoxygenation [40][41][42][43][44][45]. Cells undergoing reperfusion and reoxygenation following hypoxia produce super oxide radical [46].…”

Section: Determinants Of In Ammatory Responsivitymentioning

confidence: 99%

An Iron-Free VMP35 Multi-nutrient Complex Modulates an Array of Homeostatic Biological Parameters: Promoting Hemoglobinization, Aerobic Metabolism, Viral Immuno-competence, and Inflammatory Regulation

Blum¹,

Downs²,

Bagchi³

et al. 2020

Preprint

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Background: Integrity of hemoglobin is a crucial determining factor for the overall health functions. Nutrient repletion therapy should be a fundamental strategy to restore the healthy properties of blood. A unique patent-pending iron-free VMP35 formulation was engineered by our laboratory to restore iron-dependent hemoglobin in anemic cells using a proprietary Prodosome® absorption technology. This formulation, containing an array of nano-emulsified botanical ingredients rich in bioflavonoids, strengthens the structural integrity of connective tissues, and potentiates immune competence, cellular aerobic metabolism, and enhances efficient regulation of inflammatory events. We discuss the intricate aspects of strong vs. fragile immunity and consequential inflammatory responses to convey a deeper understanding of the varied and overly complex sequela of immunological behaviors and events. The effect of the VMP35 is mediated through highly absorbable nutritional/nutrigenomic repletion enabling improvements in the systemic set of functional behaviors. In fact, the iron-free VMP35 facilitates a “Systems Biology Approach” which restores hemoglobin status, reverses anaerobic hypoxia, improves competent immune responsivity, and regulates appropriate and controlled activation of inflammatory sequela. Under these pathogenic circumstances, iron-deficiency anemia has been misconceptualized, and a new nosological term, Chronic Anemia Syndrome, is proposed. The comparative therapeutic rationale of Reductionist vs. Systems Biology approaches is also explained in detail. Methods: The efficacy of the novel therapeutic iron-free VMP35 liquid nutraceutical is detailed in restoring iron-dependent hemoglobin to RBCs and boosting cellular morphology, viability, and immune competence, thereby reducing the need for prolonging inflammatory sequela. Results: This was demonstrated in a previous IRB approved multi-subject human study. In addition, two recent case studies report dramatic restorative benefits of nutrient repletion therapy of the VMP35 on subjects having experienced near-fatal events, which confirmed the findings explained in this manuscript. Conclusions: This novel iron-free VMP35 modulates an array of homeostatic biological parameters such as enhanced hemoglobinization, aerobic metabolism, viral immuno-competence, and inflammatory regulation. Further research, examining mechanistic and beneficial effects in athletic performance, is in progress. Importantly, during these troubled immune challenging times, modulating an array of homeostatic immunological and inflammatory dysfunctions are tantamount to improved population outcomes. Trial Registration: The Clinical investigation in a total of 38 subjects was conducted under an Institutional Review Board (IRB) from the Path Foundation in New York, NY (#13-009 April 25, 2013). The two case studies were done at Lancaster General Hospital, Lancaster, PA, and Jefferson University Hospital, Philadelphia, PA, USA. Both studies were retrospectively registered.

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Modulation of monocyte chemoattractant protein-1 expression by ischaemic preconditioning in a lung autotransplant model

Abstract: In this model, LIRI induced the expression of MCP-1 and the proinflammatory proteins TNF-α and IL-1 in control lungs. IP significantly reduced the expression of these chemokines and cytokines. These features may explain the reduction of oxidative stress observed with IP.

Cited by 8 publications

References 21 publications

Creatine supplementation attenuates pulmonary and systemic effects of lung ischemia and reperfusion injury

Creatine supplementation attenuates pulmonary and systemic effects of lung ischemia and reperfusion injury

Review 2: Primary graft dysfunction after lung transplant—pathophysiology, clinical considerations and therapeutic targets

An Iron-Free VMP35 Multi-nutrient Complex Modulates an Array of Homeostatic Biological Parameters: Promoting Hemoglobinization, Aerobic Metabolism, Viral Immuno-competence, and Inflammatory Regulation

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