Cytokine up-regulation in ischaemic/reperfused lungs perfused with University of Wisconsin solution and normal saline

2001 ◽  
Vol 101 (3) ◽  
pp. 285-294 ◽  
Author(s):  
Chi-Huei CHIANG ◽  
Cheng-Ping YU ◽  
Chin-Pyng WU ◽  
Horng-Chin YAN ◽  
Wann-Cherng PERNG
Keyword(s):  
Lung Injury ◽  
Pulmonary Oedema ◽  
Normal Saline ◽  
Cytokine Production ◽  
Interleukin 1 ◽  
Lung Weight ◽  
University Of Wisconsin Solution ◽  
University Of Wisconsin ◽  
Tnf Α ◽  
Wisconsin Solution

Ischaemia/reperfusion (I/R) lung injury using University of Wisconsin solution (UW) as perfusate has not been well studied. Isolated rat lungs were challenged with various periods of ischaemia and/or reperfusion. Haemodynamics, lung weight gain (LWG), capillary filtration coefficient (Kfc), tissue pathology, the concentrations of cytokines in the perfusate, and mRNAs for the various cytokines in the lung tissues were measured. I/R induced a permeability type of pulmonary oedema, as reflected by increases in LWG and Kfc. LWG and Kfc in the I45R60(UW) group (45 min of ischaemia followed by 60 min of reperfusion with UW) were only 2% and 5% respectively of those in the I45R60(NS) group (where NS is normal saline). LWG and Kfc in the UW group had both increased by 180 min, to values similar to those in the I45R60(NS) group. However, these findings show that UW was remarkably effective at preventing LWG after 60 min of reperfusion, and was more than 3-fold more effective than NS in delaying LWG. For longer ischaemic times only, or the same period of ischaemia followed by longer reperfusion periods, greater lung injury occurred. I/R lung injury also induced increased concentrations of tumour necrosis factor-α (TNF-α), interleukin 1 and interleukin 6 in the perfusate, and increased the mRNAs for these cytokines in lung tissue. A significant correlation was obtained between TNF-α concentration and LWG. TNF-α production in the I45R60(UW) group was only 7% of that in the I45R60(NS) group. However, TNF-α mRNA expression in the I45R60(UW) group was 80% of that in the I45R60(NS) group. This indicates that transcription/translation do not correlate well with cytokine production, and also suggests that one reason for the effectiveness of UW in delaying LWG may be because it delays TNF-α production. In summary, ischaemia or I/R caused a permeability-type pulmonary oedema that was associated with leucocyte infiltration and the up-regulation of various cytokines, regardless of the perfusion fluid. Except for pulmonary hypertension, less severe I/R lung injury and delayed cytokine production in lungs perfused with UW, the pattern of injury associated with I/R challenge was similar to that in lungs perfused with NS. We propose that more or long-acting protective agents are required as additives in order to modify UW to produce an optimal preservation solution.

Cytokine up-regulation in ischaemic/reperfused lungs perfused with University of Wisconsin solution and normal saline

2001 ◽  
Vol 101 (3) ◽  
pp. 285 ◽  
Author(s):  
Chi-Huei CHIANG ◽  
Cheng-Ping YU ◽  
Chin-Pyng WU ◽  
Horng-Chin YAN ◽  
Wann-Cherng PERNG
Keyword(s):  
Normal Saline ◽  
University Of Wisconsin Solution ◽  
University Of Wisconsin ◽  
Wisconsin Solution

Use of anti-(tumour necrosis factor-α) antibody or 3-deaza-adenosine as additives to promote protection by University of Wisconsin solution in ischaemia/reperfusion injury

2000 ◽  
Vol 99 (3) ◽  
pp. 215-222 ◽  
Author(s):  
Chi-Huei CHIANG ◽  
Chin-Pyng WU ◽  
Wann-Cherng PERNG ◽  
Horng-Chin YAN ◽  
Cheng-Ping YU
Keyword(s):  
Lung Injury ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
University Of Wisconsin ◽  
Ischaemia Reperfusion ◽  
Tnf Α ◽  
Factor Α ◽  
Wisconsin Solution ◽  
Necrosis Factor

Experimental interventions that reduce ischaemia/reperfusion (I/R) lung injury can be used to improve the properties of preservation solutions. We attempted to increase the attenuation of I/R injury by University of Wisconsin solution (UW) by adding an antibody against tumour necrosis factor-α (TNF-α), to neutralize TNF-α, and/or by adding 3-deaza-adenosine (c3-Ado), to inhibit leucocyte adhesion and the biosynthesis of ICAM-1 (intercellular cell-adhesion molecule 1). We examined I/R injury using an isolated rat lung model. Six different solutions were perfused individually, followed by evaluation of I/R injury: (1) 0.9% NaCl (normal saline; NS), (2) NS+anti-TNF-α antibody, (3) UW alone, (4) UW+anti-TNF-α, (5) UW+c3-Ado and (6) UW+anti-TNF-α+c3-Ado. Haemodynamic changes, lung weight gain, capillary filtration coefficient, TNF-α levels and lung pathology were analysed in order to evaluate I/R injury. Compared with lungs perfused with NS, lungs treated with NS+anti-TNF-α showed less I/R injury. The addition of anti-TNF-α and/or c3-Ado to UW reduced I/R injury compared with unmodified UW. Among the six solutions tested, UW containing anti-TNF-α antibody reduced I/R injury to the greatest extent. We conclude that addition of anti-TNF-α antibody or c3-Ado protects against I/R lung injury when using UW. Further investigation of the improved properties of modified UWs would be beneficial with regard to lung transplantation research.

Protective agents used as additives in University of Wisconsin solution to promote protection against ischaemia–reperfusion injury in rat lung

1998 ◽  
Vol 95 (3) ◽  
pp. 369-376
Author(s):  
Chi-Huei CHIANG ◽  
Kerry WU ◽  
Cheng-Ping YU ◽  
Wann-Cherng PERNG ◽  
Horng-Chin YAN ◽  
...  
Keyword(s):  
Weight Gain ◽  
Lung Injury ◽  
Reperfusion Injury ◽  
Protective Agent ◽  
Ischaemia Reperfusion Injury ◽  
Lung Weight ◽  
Protective Agents ◽  
University Of Wisconsin ◽  
Ischaemia Reperfusion ◽  
Wisconsin Solution

1.An intervention to reduce ischaemia–reperfusion lung injury will be an important advance in transplant medicine. Although the mechanisms associated with producing ischaemia–reperfusion endothelial injury have not been completely elucidated, many of the injury mediators have been studied in detail. While no single pharmacological therapy is likely to be totally effective in eliminating this complex injury, we have developed a mixture of agents that are known to block pathways involved in producing ischaemia–reperfusion-associated lung vascular injury. 2.The present study modified University of Wisconsin solution (UW) by adding one of the protective agents prostaglandin E1 (PGE1), dexamethasone (Dex) or dibutyryl cAMP (Bt2-cAMP), or a combination of these, to the perfusate of rat lungs exposed to 4 ;h of cold ischaemia followed by 1 ;h of reperfusion. Nine modified UW solutions were studied: (1) UW+Dex, (2) UW+PGE1, (3) UW+Bt2-cAMP, (4) UW+Dex×3, (5) UW+PGE1×3, (6) UW+Bt2-cAMP×3, (7) UW+Dex+PGE1, (8) UW+Dex+Bt2-cAMP, (9) UW+PGE1+Bt2-cAMP. These solutions were utilized in individual experiments to assess haemodynamic changes, lung weight gain, the capillary filtration coefficient (Kfc) and pathology in all lungs. 3.The results indicate that lung weight gain and Kfc values were significantly lower than with UW alone in groups 1, 2 and 3, which contained only one additional protective agent. In groups 4, 5 and 6, which contain three times the concentration of each protective agent, both Kfc and lung weight gain were similar to those measured in groups 1, 2 and 3, i.e. lungs were protected but the protection was not dose dependent. In groups 7, 8 and 9, which contained two protective agents, lung weight gain and Kfc were greatly reduced compared with UW alone. Histopathological studies showed similar decreases in the injury profiles of lungs. 4.Although UW contains several antioxidant protective agents such as allopurinol and glutathione, it did not provide effective protection in our ischaemia–reperfusion lung injury model. UW modified with an additive of PGE1, Dex or Bt2-cAMP attenuated ischaemia–reperfusion injury. Furthermore, UW containing two of these protective agents augmented the protection. Among the modified solutions, it appears that UW+PGE1+Bt2-cAMP protects the lungs to a greater extent than all other solutions used in our study. We suggest that preservation solutions containing PGE1-Bt2-cAMP will provide additional protective effects to organs stored for transplantation.

Protection of the rat liver against rewarming ischemic injury by University of Wisconsin solution

2001 ◽  
Vol 386 (1) ◽  
pp. 31-37 ◽  
Author(s):  
M. Lutterová ◽  
M. Kukan ◽  
K. Vajdová ◽  
D. Kuba ◽  
C. Mišlanová ◽  
...  
Keyword(s):  
Rat Liver ◽  
Ischemic Injury ◽  
University Of Wisconsin Solution ◽  
University Of Wisconsin ◽  
Wisconsin Solution

Clinical significance of cytokine markers in children with different courses of community-acquired pneumonia

2020 ◽  
Vol 15 (5) ◽  
pp. 18-23
Author(s):  
G.P. Evseeva ◽  
◽  
G.N. Kholodok ◽  
S.V. Pichugina ◽  
S.V. Suprun ◽  
...  
Keyword(s):  
Cytokine Production ◽  
Interleukin 1 ◽  
Interferon Γ ◽  
Peripheral Blood Lymphocytes ◽  
Community Acquired Pneumonia ◽  
Enzyme Linked Immunosorbent Assay ◽  
Interleukin 17 ◽  
Monocyte Chemoattractant Protein 1 ◽  
Tnf Α ◽  
Ifn Γ

Principles of the diagnosis and treatment of community-acquired pneumonia (CAP) in children were developed and clearly formulated long ago. Nevertheless, clinicians often encounter the problem of pulmonary and pleural complications of CAP, which is challenging in terms of the choice of initial therapy, since the first symptoms of uncomplicated and complicated pneumonia are often similar. Therefore, the search for early markers of complicated CAP in children is highly important. Objective. To assess prognostic values of spontaneous and mitogen-induced cytokine production in children with CAP. Patients and methods. We have performed comprehensive examination of 108 children with CAP. Eighty-four of them had uncomplicated CAP, whereas 24 children had CAP complicated by pleurisy. We measured spontaneous and induced production of the following cytokines upon patient admission to hospital: interleukin-1 (IL-1), interleukin-17 (IL-17), interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), and monocyte chemoattractant protein-1 (MCP-1). To measure induced cytokine production, we stimulated peripheral blood lymphocytes by S. рneumonае (serotype 7, 11; strains 7C and 11AD). The level of cytokines was evaluated using the enzyme-linked immunosorbent assay (Vektor-BEST, Novosibirsk, Russia). Results. We found that in children with uncomplicated CAP, induction of immunocompetent blood cells (IBCs) led to increased secretion of first-generation cytokines, including IL-1, TNF-α, and IFN-γ, whereas IBCs of patients with complicated CAP primarily produced second-generation cytokines, including VEGF, МРС-1, and IL-17. Conclusion. The observed differences in spontaneous and mitogen-induced cytokine production between children with and without CAP complications suggest that these parameters can be considered as promising prognostic markers for complicated CAP in children. The proposed method can be used in pediatric practice to predict the development of complications in children with CAP. Key words: children, community-acquired pneumonia, cytokines

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