Lipopolysaccharide Challenge Induces Long Pentraxin 3 Expression in Mice Independently from Acute Lung Injury<sup>△</sup>

Zeng Gao; Liu Jie; Wu Ning; Jia Cong-wei; Guo Shu-bin

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Lipopolysaccharide Challenge Induces Long Pentraxin 3 Expression in Mice Independently from Acute Lung Injury^△

Chinese Medical Sciences Journal Vol. 30, Issue 1, Pages: 7-17(2015)

Orginal Article | Updated：2024-04-10

- Lipopolysaccharide Challenge Induces Long Pentraxin 3 Expression in Mice Independently from Acute Lung Injury^△
- Affiliations：
  
  1. 1Department of Emergency Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China;
  3. 3Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China;
  2. 2Department of Thoracic Surgery, Huashan Hospital, Fudan University, Shanghai 200040, China
- Author bio：
  
  *Corresponding author E-mail: Guosb@pumch.cn
- Funds：
- DOI：
  CLC：
- Received：02 September 2014，
  
  Published Online：20 February 2015，
  
  Published：2015-02
- Accepted：
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Zeng Gao, Liu Jie, Wu Ning, et al. Lipopolysaccharide Challenge Induces Long Pentraxin 3 Expression in Mice Independently from Acute Lung Injury^△[J]. Chinese medical sciences journal, 2015, 30(1): 7-17.
DOI：

Zeng Gao, Liu Jie, Wu Ning, et al. Lipopolysaccharide Challenge Induces Long Pentraxin 3 Expression in Mice Independently from Acute Lung Injury^△[J]. Chinese medical sciences journal, 2015, 30(1): 7-17. DOI：

摘要

Abstract

Objective

To 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.

Methods

Wild-type C57BL/6 mice (12-14 weeks old) were randomly divided into 3 groups. Mice in the group 1 (

=12) and group 2 (

=12) were instilled with lipopolysaccharide

via

intratracheal or intraperitoneal routes

respectively. Mice in the group 3 (

=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).

Results

ALI 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.

Conclusions

Lipopolysaccharide 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

关键词

Keywords

references

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