Lipopolysaccharide challenge induces long pentraxin 3 expression in mice independently from acute lung injury.

Gao ZENG; Jie LIU; Ning WU; Cong-wei JIA; Shu-bin GUO

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Lipopolysaccharide challenge induces long pentraxin 3 expression in mice independently from acute lung injury.

Author: Gao ZENG ¹ ; Jie LIU ¹ ; Ning WU ² ; Cong-wei JIA ³ ; Shu-bin GUO ¹
Author Information

1. Department of Emergency Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China.
2. Department of Thoracic Surgery, Huashan Hospital, Fudan University, Shanghai 200040, China.
3. Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China.
Publication Type:Journal Article
MeSH: Acute Lung Injury; metabolism; Animals; Blotting, Western; C-Reactive Protein; metabolism; DNA Primers; Enzyme-Linked Immunosorbent Assay; Lipopolysaccharides; administration & dosage; Male; Mice; Mice, Inbred C57BL; Nerve Tissue Proteins; metabolism; Real-Time Polymerase Chain Reaction; Up-Regulation
From: Chinese Medical Sciences Journal 2015;30(1):7-17
CountryChina
Language:English
Abstract:
OBJECTIVETo determine whether the onset of acute lung injury (ALI) induces the up-regulation of pentraxin 3 (PTX3) expression in mice and whether PTX3 concentration in the biofluid can help recognizing sepsis-induced ALI.
METHODSWild-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 ALI. 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).
RESULTSALI 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 ALI evidenced by its small AUROCC. PTX3 concentration in bronchoalveolar lavage fluid did not correlate with that in serum.
CONCLUSIONSLipopolysaccharide challenges induced PTX3 expression in mice regardless of the presence of ALI. PTX3 may act as an indicator of inflammatory response instead of organ injury per se.