The role of proinflammatory cytokines in lung ischemia-reperfusion injury

Krishnadasan, Baiya; Naidu, Babu; Byrne, Karen; Fraga, Charles H.; Verrier, Edward D.; Mulligan, Michael S.

doi:10.1067/mtc.2003.16

Cited by 133 publications

(112 citation statements)

References 23 publications

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“…However, the failure of the prior physical training programme to affect lung IR-induced neutrophil influx (as assessed by measurement of MPO activity) is intriguing, especially since TNF-a plays critical roles in the regulation of neutrophil influx following lung IR injury [6,30]. Polymorphonuclear neutrophils are know to release toxic oxygen metabolites, such as superoxide anion, hydroxyl radical and hydrogen peroxide, all of which can produce cellular oxidative damage in pulmonary endothelial and parenchymal cells [31].…”

Section: Discussionmentioning

confidence: 99%

“…The present data show that the number of mononuclear and polymorphonuclear cells in trained rats (86¡3610 6 Measurement of right lung MPO activity was carried out in order to evaluate neutrophil infiltration into lung tissue. Figure 1b shows that lung IR caused a significant increase in MPO activity compared with the sham group that remained unaltered in trained rats.…”

Section: Peripheral Leukocyte Countsmentioning

confidence: 99%

“…Acute respiratory distress syndrome (ARDS) is defined as a clinical disorder associated with a systemic inflammatory response and multiple organ failure, showing a high mortality rate (40-60%) strongly associated with lung injury [5,6]. It is well known that ischaemia-reperfusion (IR) causes tissue damage and cellular dysfunction in local and remote regions, leading to ARDS and multiple organ failure [7].…”

Section: Abstract: Exercise Training Inflammation Ischaemia-reperfumentioning

confidence: 99%

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Exercise training reduces pulmonary ischaemia-reperfusion-induced inflammatory responses

Mussi¹,

Camargo²,

Ferreira³

et al. 2008

European Respiratory Journal

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Physical exercise reduces the deleterious effects of cardiovascular and inflammatory disorders. The purpose of the present study was to evaluate the beneficial effects of physical training on the inflammatory responses following lung ischaemia-reperfusion (IR) in rats.Male Wistar rats were divided into sham-operated animals and sedentary and trained animals submitted to lung IR. The run training programme consisted of 5 sessions?week , at 66% of maximal oxygen consumption for 8 weeks. The left pulmonary artery, bronchus and pulmonary vein were occluded for 90 min and reperfused for 2 h. Lung protein extravasation was measured as 125 I-human albumin accumulation, whereas lung neutrophil infiltration was measured as myeloperoxidase activity. Lung IR in sedentary rats resulted in marked increases in protein extravasation and neutrophil influx, and in significant elevations of serum tumour necrosis factor (TNF)-a and interleukin (IL)-1b levels. Physical preconditioning attenuated the increased IR-induced protein leakage without affecting neutrophil influx. It also reduced serum TNF-a (and IL-1b) levels, but had no effect on IL-10 levels. Plasma superoxide dismutase activity was significantly increased in trained IR rats.The present data show that physical preconditioning protects the rat lung from ischaemiareperfusion injury by attenuating the pulmonary vascular permeability that may be a consequence of reduced levels of tumour necrosis factor-a and interleukin-1b and elevated superoxide dismutase activity.

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Section: Discussionmentioning

confidence: 99%

Section: Peripheral Leukocyte Countsmentioning

confidence: 99%

Section: Abstract: Exercise Training Inflammation Ischaemia-reperfumentioning

confidence: 99%

See 1 more Smart Citation

Exercise training reduces pulmonary ischaemia-reperfusion-induced inflammatory responses

Mussi¹,

Camargo²,

Ferreira³

et al. 2008

European Respiratory Journal

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“…Proinflammatory cytokines, such as IL-1, tumor necrosis factor ␣ (TNF-␣), and IL-6 play a pivotal role in IRI and cellular trafficking (49). These effects are modulated by the elaboration of antiinflammatory cytokines IL-4 and IL-10 (50).…”

Section: Early Graft Dysfunctionmentioning

confidence: 99%

Lung Transplantation: Opportunities for Research and Clinical Advancement

Wilkes¹

2006

Am J Respir Crit Care Med

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Lung transplantation is the only definitive therapy for many forms of end-stage lung diseases. However, the success of lung transplantation is limited by many factors: (1 ) Too few lungs available for transplantation due to limited donors or injury to the donor lung; (2 ) current methods of preservation of excised lungs do not allow extended periods of time between procurement and implantation; (3 ) acute graft failure is more common with lungs than other solid organs, thus contributing to poorer short-term survival after lung transplant compared with that for recipients of other organs; (4 ) lung transplant recipients are particularly vulnerable to pulmonary infections; and (5 ) chronic allograft dysfunction, manifest by bronchiolitis obliterans syndrome, is frequent and limits long-term survival. Scientific advances may provide significant improvements in the outcome of lung transplantation. The National Heart, Lung, and Blood Institute convened a working group of investigators on June 14-15, 2004, in Bethesda, Maryland, to identify opportunities for scientific advancement in lung transplantation, including basic and clinical research. This workshop provides a framework to identify critical issues related to clinical lung transplantation, and to delineate important areas for productive scientific investigation. Keywords: allograft dysfunction; infection; ischemia-reperfusion injury; lung transplantation; obliterative bronchiolitis; rejectionThe transplantation of organs offers the promise of life-saving and life-enhancing therapy for a variety of ailments. Lung transplantation (LTx) has become an acceptable therapy to palliate patients with a variety of end-stage lung diseases. However, lung transplantation has not turned out to be a panacea for chronic lung disease because of significant limitations in the entire transplant process (Figure 1). First, there are not nearly enough suitable donor lungs to meet the needs of all patients with end-stage lung disease. As a result, more patients die waiting for transplants than from mortality associated with a lung transplant. Second, early graft survival after LTx is worse than for other types of organs transplanted (1). Finally, late survival after successful LTx is hampered by the development of chronic allograft dysfunction and by the life-limiting complications associated with conventional immunosuppressive medications. Two factors impede progress to address these problems: (1 ) lung transplant centers lack the infrastructure to facilitate prospective, multicenter clinical studies of sufficient power to address clinical questions and (2 ) there are too few investigators studying the biology of lung transplantation.The NHLBI convened a workshop on June 14-15, 2004, to better understand these complex problems and to identify strategies to address these and prioritize them. The topics addressed by participants were wide-ranging. They included the following: lung use rates from conventional brain-dead organ donors; safe limits for donor lung function; consideration o...

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“…In addition to serving as chemotactic factors, C-C chemokines can modulate cytokine production, adhesion molecule expression, and mononuclear cell proliferation. Krishnadasan et al demonstrated that TNF-α and IL-1β promote lung IR injury likely by altering the expression of other pro-inflammatory cytokines and by influencing neutrophil recruitment (Krishnadasan, et al, 2003). Antibodies to TNF-α, IFN-γ, and MCP-1 have been utilized to demonstrate the importance of these mediators in lung IR injury (Eppinger, et al, 1997).…”

Section: Cytokines and Chemokinesmentioning

confidence: 99%