Changes of selected systemic cytokines in severe pediatric lung disease
Authors:
L. Šašek; J. Fremuth; K. Pizingerová; J. Kobr
Authors‘ workplace:
Dětská klinika, Univerzita Karlova v Praze, Lékařská fakulta a Fakultní nemocnice v Plzni
přednosta prof. MUDr. J. Sýkora, Ph. D.
Published in:
Čes-slov Pediat 2016; 71 (5-6): 251-259.
Category:
Original Papers
Overview
Background:
Severe lung diseases leading to respiratory failure are among the most frequent causes of critical conditions in childhood. Pulmonary injury leads to a systemic response of the organism and the response rate should be at the level of cytokines proportional to the degree of lung injury. The study aims to monitor systemic inflammatory response dependence on the degree of pulmonary injury using selected cytokines in pediatric patients.
Methods:
Thirty-two patients with severe pulmonary injury and Lung Injury Score >1.0 leading to respiratory failure were included. Mean age of enrolled patients was 39.5 months, weight 14.2 kg. Twenty-nine patients had primary lung disease ALI//ARDS based on aspiration, pulmonary infection, autoimmune process, pulmonary contusion, or pulmonary arterial hypertension, 3 patients secondary ARDS in septic shock and multiorgan failure. Patients were mechanically invasively ventilated. Patients were monitored during the study for 48 hours, laboratory sampling was performed in the 1st, 12th, 24th and 48th hour of experiment.
Results:
From observed markers matrix metalloproteinase MMP-9 was extremely high already in 1st hour with subsequent significant decrease. There was counter-regulatory increase of metalloproteinases inhibitor TIMP-1 at 12th hour related to initially high MMP-9. Expression of adhesion molecules was present already at the beginning of observation. ICAM-1 during the study descend insignificantly. VCAM-1 changes over time were statistically very significant with initial high levels and further decreasing the expression.
Conclusions:
On the set of critically ill children with severe pulmonary impairment were detected early systemic cytokine response with signs of endothelial activation. Changes in the spectrum of cytokines in severe lung disease may indicate the influence of other organ systems, not only on the level of blood gases exchange alterations resulting in tissue hypoxia.
Key words:
ALI, ARDS, adhesion molecules, metalloproteinases
Sources
1. Dreyfuss DE, Saumon G. Ventilator-induced lung injury. Am J Respir Crit Care Med 1998 Jan; 157 (1): 294–323.
2. de Prost N, Costa EL, Wellman T. Effect of ventilation strategy on distribution of lung inflammatory cell activity. Crit Care 2013; 17 (4): R175.
3. Pierrakos Ch, Vincent JL. Sepsis biomarkers: a review. Crit Care 2010, 14(1): R15.
4. Warre LB, Koyama T, Zhao Z. Biomarkers of lung epithelial injury and inflammation distinguish severe sepsis patients with acute respiratory distress syndrome. Crit Care 2013; 17 (5): R253.
5. Lee, I, Yang Ch. Inflammatory signaling involved in airway and pulmonary diseases. Mediators Inflamm 2013; 791231.
6. Schutte H, Lohmeyer J, Rousseau S. Bronchoalveolar and systemic cytokine profiles in patients with ARDS, severe pneumonia and cardiogenic pulmonary edema. Eur Respir J 1996; 9 (9): 1858–1867.
7. Hsu AT, Barett CD, DeBusk GM, et al. Kinetics and role of plasma matrix metalloproteinase-9 expression in acute lung injury and the acute respiratory distress syndrome. Shock 2015; 44 (2): 128–136.
8. Krueger M, Heinzmann A, Nauck M. Adhesion molecules in pediatric intensive care patients with organ dysfunction syndrome. Intensive Care Med 2007; 33 (2): 359–363.
9. Tabuchi A, Kuebler WM. Endothelium-platelet interactions in inflammatory lung disease. Vasc Pharmacol 2008; 49 (4–6): 141–150.
10. Xing K, Murthy S, Liles CW. Clinical utility of biomarkers of endothelial activation in sepsis - a systematic review. Crit Care 2012; 16 (1): R7.
11. Zonneveld R, Martinelli R, Shapiro NI. Soluble adhesion molecules as markers for sepsis and the potential pathophysiological discrepancy in neonates, children and adults. Crit Care 2014; 18 (1): 204.
12. Fligiel S, Standiford T, Fligiel H, et al. Matrix metalloproteinases and matrix metalloproteinase inhibitors in acute lung injury. Hum Pathol 2006; 37 (4): 422–430.
13. Kim JH, Suk MH, Youn DW, et al. Inhibition of matrix metalloproteinase-9 prevents neutrophilic inflammation in ventilator-induced lung injury. Am J Physiol Lung Cell Mol Physiol 2006; 291 (4): L580–L587.
14. Greenlee KJ, Werb Z, Kheradmand F. Matrix metalloproteinases in lung. Physiol Rev 2007; 87 (1): 69–98.
15. Lorente L, Martin MM, Labarta L. Matrix metalloproteinase-9,-10, and tissue inhibitor of matrix metalloproteinases-1 blood level as biomarkers of severity and mortality in sepsis. Crit Care 2009; 13 (5): R158.
16. Kong M, Li Y, Gaggar A. Matrix metalloproteinase activity in pediatric acute lung injury. Int J Med Sci 2009; 6 (1): 9–17.
17. Lagente V, Boichot E. Role of matrix metalloproteinases in the inflammatory process of respiratory diseases. J Mol Cell Cardiol 2010; 48 (3): 440–444.
18. Cena, JJ, Lalu MM, Cho WJ, et al. Inhibition of matrix metalloproteinase activity in vivo protects against vascular hyporeactivity in endotoxemia. Am J Physiol Heart Circ Physiol 2010; 298 (1): H45–H51.
19. Lauhio A, Hastbacka J, Pettila V, et al. Serum MMP-8,-9 and TIMP-1 in sepsis. Pharmacol Res 2011, 64 (6): 590–594.
20. Davey A, McAuley DF, O’Kane CM. Matrix metalloproteinases in acute lung injury: mediators of injury and drivers of repair. Eur Respir J 2011; 38 (4): 959–970.
21. Yazdan-Ashoori P, Liaw P, Toltl L, et al. Elevated plasma matrix metalloproteinases and their tissue inhibitors in patients with severe sepsis. J Crit Care 2011; 26 (6): 556–565.
22. Li J, Zhong J, Liu H, et al. Imbalance between tissue inhibitor of metalloproteinase 1 and matrix metalloproteinase 9 after cardiopulmonary resuscitation. Am J Emerg Med 2012; 30 (7): 1202–1209.
23. Teng L, Yu M, Li J. Matrix metalloproteinase-9 as a new biomarkers of severity in multiple organ dysfunction syndrome caused by trauma and infection. Mol Cell Biochem 2012; 360 (1–2): 271–277.
24. Yamamoto Y, Osanai T, Nishizaki F, et al. Matrix metalloprotein-9 activation under cell-to-cell interaction between endothelial cells and monocytes. Heart Vessels 2012; 27 (6): 624–633.
25. Bradley LM, Douglass MF, Chatterjee D, et al. Matrix metalloproteinase 9 mediates neutrophil migration into the airways in response to influenza virus-induced toll-like receptor signaling. PLoS Pathog 2012; 8 (4): e1002641.
26. Herzig DS, Driver BR, Fang G, et al. Therapeutic efficiacy of CXCR3 blockade in an experimental model of severe sepsis. Crit Care 2012; 16 (5): R168.
27. Kobr J, Pizingerova K, Fremuth J, et al. Signaling molecules for early detection of adverse interactions during mechanical ventilation in animal models. In Vivo 2011; 25 (2): 209–217.
28. Kobr J, Fremuth J, Pizingerova K, et al. Total body response to mechanical ventilation of healthy lungs: an experimental study in piglets. Physiol Res 2010; 59 (4): 545–552.
29. Kobr J, Kuntscher V, Molacek K, et al. Diffuse alveolar damage due to inappropriate strategy of mechanical ventilation in an experimental porcine model. In Vivo 2010; 24 (5): 699–704.
30. Kobr J, Kuntscher V, Treska V, et al. Adverse effects of the high tidal volume during mechanical ventilation of normal lung in pigs. Bratisl Lek Listy 2008; 109 (2): 45–51.
31. Kobr J, Fremuth J, Pizingerova K, et al. Vliv ventilace trvalým pozitivním tlakem na stupeň zánětlivé reakce a funkce orgánů – experimentální studie. Anest intenziv Med 2009; 20 (2): 88–95.
Labels
Neonatology Paediatrics General practitioner for children and adolescentsArticle was published in
Czech-Slovak Pediatrics
2016 Issue 5-6
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