Document Detail

Inflammation and Matrix remodelling during repair of Ventilator-induced lung injury.
MedLine Citation:
PMID:  21743031     Owner:  NLM     Status:  Publisher    
High-pressure ventilation triggers different inflammatory and matrix remodeling responses within the lung. Although some of them may cause injury, the involvement of these mediators in repair is largely unknown. To identify mechanisms of repair after ventilator-induced lung injury (VILI), mice were randomly assigned to baseline conditions (no ventilation), injury (90 minutes of high-pressure ventilation without PEEP), repair (injury followed by 4 hours of low-pressure ventilation with PEEP) and ventilated controls (low-pressure ventilation with PEEP for 90 and 330 minutes). Histological injury and lung permeability increased during injury, but were partially reverted in the repair group. This was accompanied by a pro-inflammatory response together with increases in TNFα and IFNγ, which returned to baseline during repair, and a decrease in IL-10. However, MIP-2 and Matrix metalloproteinases (MMP) -2 and -9 increased after injury and persisted elevated during repair. Mortality in the repair phase was 50%. Survivors showed increased cell proliferation, lower levels of collagen and higher levels of MIP-2 and MMP-2. PanMMP or specific MMP-2 inhibition (but not MIP-2, TNFα or IL-4 inhibition), delayed epithelial repair in an in vitro wound model using murine or human alveolar cells cultured in the presence of BALF from mice during the repair phase or from patients with ARDS, respectively. Similarly, MMP inhibition with doxycycline impaired lung repair after VILI in vivo. In conclusion, VILI can be reverted by normalizing ventilation pressures. An adequate inflammatory response and extracellular matrix remodeling are essential for recovery. MMP-2 could play a key role in epithelial repair after VILI and ARDS.
Adrián González-López; Aurora Astudillo; Emilio Garcia-Prieto; María Soledad Fernández-García; Antonio López-Vazquez; Estefanía Batalla-Solís; Francisco Taboada; Antonio Fueyo; Guillermo M Albaiceta
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-7-8
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  -     ISSN:  1522-1504     ISO Abbreviation:  -     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-7-11     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
1Universidad de Oviedo.
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