Pentraxin 3 accelerates lung injury in high tidal volume ventilation in mice

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• 作者：Juliana Monte Real^a ; ^b ; ^{juliana_mreal@yahoo.com.br} ; Graziela Machado Gruner Turco Spilborghs^b ; ^{spilborghs@accamargo.org.br} ; Mariana Morato-Marques^b ; ^{marimorato@gmail.com} ; Ricardo Pereira de Moura^a ; ^c ; ^{rmoura@ludwig.org.br} ; Elnara Marcia Negri^d ; ^{emnegri@yahoo.com.br} ; Anamaria Aranha Camargo^a ; ^c ; ^{anamaria@ludwig.org.br} ; Daniel Deheinzelin^a ; ¹ ; ^{ddeheinz@uol.com.br} ; Adriana Abalen Martins Dias^b ; ^e ; ¹ ; ^{abalen@yahoo.com}
• 关键词：ARDS ; acute respiratory distress syndrome ; Ccl2 ; chemokine (C-C motif) ligand 2 (also known as monocyte chemoatractant protein/Mcp1) ; CRP ; C-reactive protein ; Cxcl1 ; chemokine (C-X-C motif) ligand 1 (also known as keratinocyte-derived chemokine/Kc) ; Hprt
• 刊名：Molecular Immunology
• 出版年：2012
• 期刊代码：112_01615890
• 类别：bio
• 出版时间：May, 2012
• 卷：51
• 期：1
• 页码：82-90
• 文件大小：905 K

摘要

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 m>Ptx3m> gene were subjected to high tidal volume ventilation (m>Vm>_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 m>Ptx3m>-overexpressing mice. m>Ptx3m> knockout and wild-type mice developed same lung injury degree in similar times (156 卤 42 min and 148 卤 41 min, respectively; m>pm> = 0.8173). However, m>Ptx3m> over-expression led to a faster development of VILI in m>Ptx3m>-overexpressing mice (77 卤 29 min m>vsm> 118 卤 41 min, m>pm> = 0.0225) which also displayed a faster kinetics of m>Il1bm> expression and elevated m>Ptx3m>, m>Cxcl1m> and m>Ccl2m> transcripts levels in comparison with wild-type mice assessed by quantitative real-time polymerase chain reaction. m>Ptx3m> deficiency did not impacted the time for VILI induced by high tidal volume ventilation but m>Ptx3m>-overexpression increased inflammatory response and reflected in a faster VILI development.