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Pentraxin 3 accelerates lung injury in high tidal volume ventilation in mice.
- Source :
-
Molecular immunology [Mol Immunol] 2012 May; Vol. 51 (1), pp. 82-90. Date of Electronic Publication: 2012 Mar 15. - Publication Year :
- 2012
-
Abstract
- Mechanical ventilation is the major cause of iatrogenic lung damage in intensive care units. Although inflammation is known to be involved in ventilator-induced lung injury (VILI), several aspects of this process are still unknown. Pentraxin 3 (PTX3) is an acute phase protein with important regulatory functions in inflammation which has been found elevated in patients with acute respiratory distress syndrome. This study aimed at investigating the direct effect of PTX3 production in the pathogenesis of VILI. Genetically modified mice deficient and that over express murine Ptx3 gene were subjected to high tidal volume ventilation (V(T)=45 mL/kg, PEEP(zero)). Morphological changes and time required for 50% increase in respiratory system elastance were evaluated. Gene expression profile in the lungs was also investigated in earlier times in Ptx3-overexpressing mice. Ptx3 knockout and wild-type mice developed same lung injury degree in similar times (156±42 min and 148±41 min, respectively; p=0.8173). However, Ptx3 over-expression led to a faster development of VILI in Ptx3-overexpressing mice (77±29 min vs 118±41 min, p=0.0225) which also displayed a faster kinetics of Il1b expression and elevated Ptx3, Cxcl1 and Ccl2 transcripts levels in comparison with wild-type mice assessed by quantitative real-time polymerase chain reaction. Ptx3 deficiency did not impacted the time for VILI induced by high tidal volume ventilation but Ptx3-overexpression increased inflammatory response and reflected in a faster VILI development.<br /> (Copyright © 2012 Elsevier Ltd. All rights reserved.)
- Subjects :
- Animals
C-Reactive Protein genetics
Chemokine CCL2 biosynthesis
Chemokine CCL2 genetics
Chemokine CXCL1 biosynthesis
Chemokine CXCL1 genetics
Disease Models, Animal
Gene Expression Profiling
Inflammation immunology
Inflammation pathology
Lung pathology
Lung physiopathology
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Serum Amyloid P-Component genetics
Tidal Volume
Ventilator-Induced Lung Injury pathology
Ventilator-Induced Lung Injury physiopathology
Ventilators, Mechanical adverse effects
C-Reactive Protein metabolism
Lung metabolism
Respiration, Artificial adverse effects
Serum Amyloid P-Component metabolism
Ventilator-Induced Lung Injury metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1872-9142
- Volume :
- 51
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Molecular immunology
- Publication Type :
- Academic Journal
- Accession number :
- 22425349
- Full Text :
- https://doi.org/10.1016/j.molimm.2012.02.113