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Correspondence  |   December 2017
What Is the Role of Cytokines during Ventilator-induced Lung Injury?
Author Notes
  • Louis Mourier Hospital, Colombes, France (D.D.). didier.dreyfuss@aphp.fr
  • (Accepted for publication September 20, 2017.)
    (Accepted for publication September 20, 2017.)×
Article Information
Correspondence
Correspondence   |   December 2017
What Is the Role of Cytokines during Ventilator-induced Lung Injury?
Anesthesiology 12 2017, Vol.127, 1041-1042. doi:10.1097/ALN.0000000000001934
Anesthesiology 12 2017, Vol.127, 1041-1042. doi:10.1097/ALN.0000000000001934
To the Editor:
We are pleased that Lex and Uhlig1  come to the same conclusion we published more than 15 yr ago,2  that the role of inflammatory cytokines is minor (if there is indeed any role at all) during ventilator-induced lung injury (VILI). However, we and Dr. Uhlig have had different perspectives on that matter for years. Indeed, in response to an article we wrote on the role of cytokines during VILI,3  Uhlig did not agree with our contention that cytokine secretion by the lungs is a by-product without physiologic significance. In contrast, he emphasized the importance of cytokine mediators in the pathogenesis of VILI.4 
We believe that the article by Lex and Uhlig1  and the accompanying editorial5  omitted some key references that illustrate the role of mediators in lung injury in a broader context. For example, cytokines might be important in VILI only in the setting of another source of inflammation,6  and von Bethmann et al.7  demonstrated that inflammatory cytokines and prostanoids may be produced by the lungs during low tidal volume (noninjurious) ventilation. Therefore it is not possible to determine the exact role of cytokines in the development of VILI, because their elevation, when observed, may be either a cause (which we think unlikely) or a consequence of lung overdistension, and the results of experimental studies (including those by Uhlig) are often inconsistent.3  Finally, even if mediators play a role in propagating lung injury, the most important clinical aspect is that simply reducing tidal volume has resulted in a marked reduction in mortality from adult respiratory distress syndrome, whereas to date all clinical trials of antimediator therapies in critically ill patients have been negative.
Competing Interests
The authors declare no competing interests.
Didier Dreyfuss, M.D., Georges Saumon, M.D. Louis Mourier Hospital, Colombes, France (D.D.). didier.dreyfuss@aphp.fr
References
Lex, D, Uhlig, S One-hit models of ventilator-induced lung injury: Benign inflammation versus inflammation as a by-product. Anesthesiology 2017; 126:909–22 [Article] [PubMed]
Ricard, JD, Dreyfuss, D, Saumon, G Production of inflammatory cytokines in ventilator-induced lung injury: A reappraisal. Am J Respir Crit Care Med 2001; 163:1176–80 [Article] [PubMed]
Dreyfuss, D, Ricard, JD, Saumon, G On the physiologic and clinical relevance of lung-borne cytokines during ventilator-induced lung injury. Am J Respir Crit Care Med 2003; 167:1467–71 [Article] [PubMed]
Uhlig, S, Ranieri, M, Slutsky, ASBiotrauma hypothesis of ventilator-induced lung injury. Am J Respir Crit Care Med 2004; 169:314–5; author reply 315 [Article] [PubMed]
Takata, M, Wilson, MR If we ask a mouse about biotrauma, will it give us a sensible answer? Anesthesiology 2017; 126:766–7 [Article] [PubMed]
Bouadma, L, Schortgen, F, Ricard, JD, Martet, G, Dreyfuss, D, Saumon, G Ventilation strategy affects cytokine release after mesenteric ischemia-reperfusion in rats. Crit Care Med 2004; 32:1563–9 [Article] [PubMed]
von Bethmann, AN, Brasch, F, Nüsing, R, Vogt, K, Volk, HD, Müller, KM, Wendel, A, Uhlig, S Hyperventilation induces release of cytokines from perfused mouse lung. Am J Respir Crit Care Med 1998; 157:263–72 [Article] [PubMed]