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The IL-33-ST2 Pathway Contributes to Ventilator-Induced Lung Injury in Septic Mice in a Tidal Volume-Dependent Manner.
Shock. 2019 09; 52(3):e1-e11.S

Abstract

Mechanical ventilation (MV) is frequently employed to manage respiratory failure in sepsis patients and is required for the surgical management of intra-abdominal sepsis. The impact of MV varies dramatically depending on tidal volume, with even moderate tidal volume (MTV) ventilation leading to ventilator-induced lung injury, whereas low tidal volume (LTV) ventilation protects against sepsis-induced acute respiratory distress syndrome. Interleukin (IL)-33 is known to contribute to lung injury in sepsis and its release can be induced by mechanical stress. To determine the relationship between the IL-33-suppression of tumorigenicity 2 (ST2) pathway and patterns of lung injury associated with MV in sepsis, mice were subjected to cecal ligation and puncture (CLP) followed 6 h later by either MTV (10 mL/kg) or LTV (6 mL/kg) ventilation for 4 h. MTV and LTV ventilation alone for 4 h had no impact on lung injury. MTV markedly exacerbated lung injury and inflammation, while LTV significantly suppressed these parameters in septic mice. Lung and plasma levels of IL-33 ST2 were significantly elevated by CLP alone at 10 h. MTV caused further and significant increases in IL-33 and sST2 levels, while LTV significantly suppressed levels induced by CLP. Deletion of IL-33 or ST2 prevented the increase in lung injury and inflammation induced by MTV in septic mice, while administration of recombinant IL-33 in the airway reversed the protection seen with LTV. Taken together, these findings implicate the IL-33-ST2 pathway in the pro-inflammatory changes induced by the mechanical ventilation that leads to lung injury in the setting of intra-abdominal sepsis in a tidal volume-dependent manner.

Authors+Show Affiliations

Department of Anesthesiology, East Hospital, Tongji University School of Medicine, Shanghai, China. Department of Anesthesiology, Renji Hospital, Jiaotong University School of Medicine, Shanghai, China. Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.Department of Anesthesiology, East Hospital, Tongji University School of Medicine, Shanghai, China. Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.Department of Anesthesiology, East Hospital, Tongji University School of Medicine, Shanghai, China.Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.Department of Anesthesiology, East Hospital, Tongji University School of Medicine, Shanghai, China.Department of Anesthesiology, East Hospital, Tongji University School of Medicine, Shanghai, China.Department of Anesthesiology, East Hospital, Tongji University School of Medicine, Shanghai, China.Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.Department of Environmental and Occupational Health, University of Pittsburgh Graduate School Public Health, Pittsburgh, Pennsylvania.Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.Department of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.Department of Anesthesiology, East Hospital, Tongji University School of Medicine, Shanghai, China. Department of Anesthesiology, Cancer Hospital Chinese Academy of Medical Sciences, Shenzhen, China.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

30192340

Citation

Ding, Xibing, et al. "The IL-33-ST2 Pathway Contributes to Ventilator-Induced Lung Injury in Septic Mice in a Tidal Volume-Dependent Manner." Shock (Augusta, Ga.), vol. 52, no. 3, 2019, pp. e1-e11.
Ding X, Jin S, Shao Z, et al. The IL-33-ST2 Pathway Contributes to Ventilator-Induced Lung Injury in Septic Mice in a Tidal Volume-Dependent Manner. Shock. 2019;52(3):e1-e11.
Ding, X., Jin, S., Shao, Z., Xu, L., Yu, Z., Tong, Y., Chen, Z., Turnquist, H., Pitt, B. R., Billiar, T. R., Zhang, L. M., & Li, Q. (2019). The IL-33-ST2 Pathway Contributes to Ventilator-Induced Lung Injury in Septic Mice in a Tidal Volume-Dependent Manner. Shock (Augusta, Ga.), 52(3), e1-e11. https://doi.org/10.1097/SHK.0000000000001260
Ding X, et al. The IL-33-ST2 Pathway Contributes to Ventilator-Induced Lung Injury in Septic Mice in a Tidal Volume-Dependent Manner. Shock. 2019;52(3):e1-e11. PubMed PMID: 30192340.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The IL-33-ST2 Pathway Contributes to Ventilator-Induced Lung Injury in Septic Mice in a Tidal Volume-Dependent Manner. AU - Ding,Xibing, AU - Jin,Shuqing, AU - Shao,Zhenzhen, AU - Xu,Li, AU - Yu,Zhuang, AU - Tong,Yao, AU - Chen,Zhixia, AU - Turnquist,Heth, AU - Pitt,Bruce R, AU - Billiar,Timothy R, AU - Zhang,Li-Ming, AU - Li,Quan, PY - 2018/9/8/pubmed PY - 2020/7/24/medline PY - 2018/9/8/entrez SP - e1 EP - e11 JF - Shock (Augusta, Ga.) JO - Shock VL - 52 IS - 3 N2 - Mechanical ventilation (MV) is frequently employed to manage respiratory failure in sepsis patients and is required for the surgical management of intra-abdominal sepsis. The impact of MV varies dramatically depending on tidal volume, with even moderate tidal volume (MTV) ventilation leading to ventilator-induced lung injury, whereas low tidal volume (LTV) ventilation protects against sepsis-induced acute respiratory distress syndrome. Interleukin (IL)-33 is known to contribute to lung injury in sepsis and its release can be induced by mechanical stress. To determine the relationship between the IL-33-suppression of tumorigenicity 2 (ST2) pathway and patterns of lung injury associated with MV in sepsis, mice were subjected to cecal ligation and puncture (CLP) followed 6 h later by either MTV (10 mL/kg) or LTV (6 mL/kg) ventilation for 4 h. MTV and LTV ventilation alone for 4 h had no impact on lung injury. MTV markedly exacerbated lung injury and inflammation, while LTV significantly suppressed these parameters in septic mice. Lung and plasma levels of IL-33 ST2 were significantly elevated by CLP alone at 10 h. MTV caused further and significant increases in IL-33 and sST2 levels, while LTV significantly suppressed levels induced by CLP. Deletion of IL-33 or ST2 prevented the increase in lung injury and inflammation induced by MTV in septic mice, while administration of recombinant IL-33 in the airway reversed the protection seen with LTV. Taken together, these findings implicate the IL-33-ST2 pathway in the pro-inflammatory changes induced by the mechanical ventilation that leads to lung injury in the setting of intra-abdominal sepsis in a tidal volume-dependent manner. SN - 1540-0514 UR - https://www.unboundmedicine.com/medline/citation/30192340/The_IL_33_ST2_Pathway_Contributes_to_Ventilator_Induced_Lung_Injury_in_Septic_Mice_in_a_Tidal_Volume_Dependent_Manner_ L2 - https://doi.org/10.1097/SHK.0000000000001260 DB - PRIME DP - Unbound Medicine ER -