title: Pentraxin 3 accelerates lung injury in high tidal volume ventilation in mice.
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.
authors.affiliation: Hospital Sírio-Libanês, São Paulo, Brazil. juliana_mreal@yahoo.com.br
authors.forename: Juliana Monte
authors.initials: JM
authors.lastname: Real
authors.forename: Graziela Machado Gruner Turco
authors.initials: GM
authors.lastname: Spilborghs
authors.forename: Mariana
authors.initials: M
authors.lastname: Morato-Marques
authors.forename: Ricardo Pereira
authors.initials: RP
authors.lastname: de Moura
authors.forename: Elnara Marcia
authors.initials: EM
authors.lastname: Negri
authors.forename: Anamaria Aranha
authors.initials: AA
authors.lastname: Camargo
authors.forename: Daniel
authors.initials: D
authors.lastname: Deheinzelin
authors.forename: Adriana Abalen Martins
authors.initials: AA
authors.lastname: Dias
mesh_terms: D000818:Animals; D002097:C-Reactive Protein / Q000235:genetics / Q000378:metabolism*; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000235:genetics; D054360:Chemokine CXCL1 / Q000096:biosynthesis / Q000235:genetics; D004195:Disease Models, Animal; D020869:Gene Expression Profiling; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D008168:Lung / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D012121:Respiration, Artificial / Q000009:adverse effects*; D000683:Serum Amyloid P-Component / Q000235:genetics / Q000378:metabolism*; D013990:Tidal Volume; D055397:Ventilator-Induced Lung Injury / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D012122:Ventilators, Mechanical / Q000009:adverse effects; D000099153:Pentraxins
chemical_list: D002097:C-Reactive Protein; D018932:Chemokine CCL2; D054360:Chemokine CXCL1; D000683:Serum Amyloid P-Component; D000099153:Pentraxins