Objective To determine whether the onset of acute lung injury （ALl） induces the up-regulation of pentraxin 3 （PTX3） expression in mice and whether PTX3 concentration in the biofluid can help recognizing sepsis-ind...Objective To determine whether the onset of acute lung injury （ALl） induces the up-regulation of pentraxin 3 （PTX3） expression in mice and whether PTX3 concentration in the biofluid can help recognizing sepsis-induced ALI. Methods Wild-type C57BL/6 mice （12-14 weeks old） were randomly divided into 3 groups. Mice in the group 1 （n=12） and group 2 （n=12） were instilled with lipopolysaccharide via intratracheal or intraperitoneal routes, respectively. Mice in the group 3 （n=8） were taken as blank controls. Pulmonary morphological and functional alterations were measured to determine the presence of experimental ALl. PTX3 expression in the lung was quantified at both protein and mRNA levels. PTX3 protein concentration in blood and bronchoalveolar lavage fluid was measured to evaluate its ability to diagnose sepsis-induced ALI by computing area under receiver operator characteristic curve （AUROCC）. Results ALl was commonly confirmed in the group 1 but never in the other groups. PTX3 expression was up-regulated indiscriminately among lipopolysaccharide-challenged mice. PTX3 protein concentration in the biofluid was unable to diagnose sepsis-induced ALl evidenced by its small AUROCC. PTX3 concentration in bronchoalveolar lavage fluid did not correlate with that in serum. Conclusions Lipopolysaccharide challenges induced PTX3 expression in mice regardless of the presence ofALI. PTX3 may act as an indicator of inflammatory response instead of organ injury per se.展开更多
基金Partly supported by a grant from Jie-shou Li Academician Gut Barrier Research Fund
文摘Objective To determine whether the onset of acute lung injury （ALl） induces the up-regulation of pentraxin 3 （PTX3） expression in mice and whether PTX3 concentration in the biofluid can help recognizing sepsis-induced ALI. Methods Wild-type C57BL/6 mice （12-14 weeks old） were randomly divided into 3 groups. Mice in the group 1 （n=12） and group 2 （n=12） were instilled with lipopolysaccharide via intratracheal or intraperitoneal routes, respectively. Mice in the group 3 （n=8） were taken as blank controls. Pulmonary morphological and functional alterations were measured to determine the presence of experimental ALl. PTX3 expression in the lung was quantified at both protein and mRNA levels. PTX3 protein concentration in blood and bronchoalveolar lavage fluid was measured to evaluate its ability to diagnose sepsis-induced ALI by computing area under receiver operator characteristic curve （AUROCC）. Results ALl was commonly confirmed in the group 1 but never in the other groups. PTX3 expression was up-regulated indiscriminately among lipopolysaccharide-challenged mice. PTX3 protein concentration in the biofluid was unable to diagnose sepsis-induced ALl evidenced by its small AUROCC. PTX3 concentration in bronchoalveolar lavage fluid did not correlate with that in serum. Conclusions Lipopolysaccharide challenges induced PTX3 expression in mice regardless of the presence ofALI. PTX3 may act as an indicator of inflammatory response instead of organ injury per se.
