嗜酸乳杆菌缓解LPS诱导的急性肺炎小鼠肺部炎症及机制研究

解浪浪; 王宗华; 王伟; 罗月; 黎宁; 陈陵

doi:10.16016/j.2097-0927.202307054

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嗜酸乳杆菌缓解LPS诱导的急性肺炎小鼠肺部炎症及机制研究

基础医学 | 更新时间：2026-01-09

- 嗜酸乳杆菌缓解LPS诱导的急性肺炎小鼠肺部炎症及机制研究
- Lactobacillus acidophilus alleviates lung inflammation in LPS-induced acute pneumonia in mice: efficacy and mechanism
- 陆军军医大学学报 2024年46卷第5期页码：450-457
- 作者机构：
  
  1.400020 重庆，陆军军医大学(第三军医大学)第一附属医院第958医院消化内科
  2.400038 重庆，陆军军医大学(第三军医大学)临床护理学教研室
  3.400038 重庆，陆军军医大学(第三军医大学)第一附属医院烧伤研究所
- 作者简介：
  
  [陈陵, E-mail：ilovepla@tom.comc CHEN Ling, E-mail: ilovepla@tom.comc
- 基金信息：
  
  重庆市自然科学基金面上项目(cstc2020jcyj-msxmX1055)
- DOI：10.16016/j.2097-0927.202307054
  中图分类号： Q939.121;R363.22;R563.1
- 收稿：2023-07-11，
  
  修回：2023-10-20，
  
  纸质出版：2024-03-15
- 稿件说明：
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解浪浪, 王宗华, 王伟, 等. 嗜酸乳杆菌缓解LPS诱导的急性肺炎小鼠肺部炎症及机制研究[J]. 陆军军医大学学报, 2024,46(5):450-457.

Langlang XIE, Zonghua WANG, Wei WANG, et al. Lactobacillus acidophilus alleviates lung inflammation in LPS-induced acute pneumonia in mice: efficacy and mechanism[J]. Journal of Army Medical University, 2024, 46(5): 450-457.
解浪浪, 王宗华, 王伟, 等. 嗜酸乳杆菌缓解LPS诱导的急性肺炎小鼠肺部炎症及机制研究[J]. 陆军军医大学学报, 2024,46(5):450-457. DOI： 10.16016/j.2097-0927.202307054.

Langlang XIE, Zonghua WANG, Wei WANG, et al. Lactobacillus acidophilus alleviates lung inflammation in LPS-induced acute pneumonia in mice: efficacy and mechanism[J]. Journal of Army Medical University, 2024, 46(5): 450-457. DOI： 10.16016/j.2097-0927.202307054.

摘要

目的

探究嗜酸乳杆菌对脂多糖(LPS)诱导的急性肺炎小鼠的炎症的影响及可能的机制。

方法

将21只小鼠分为对照组(NC)、模型组(LPS)和嗜酸乳杆菌处理组(Probiotics)。NC组(

=6)小鼠正常喂养，LPS组(

=8)和Probiotics组(

=7)小鼠采用LPS(10 mg/kg)气管滴注法建立急性肺炎小鼠模型，Probiotics组小鼠给予嗜酸乳杆菌，7 d后处死小鼠。通过HE染色、肺组织湿/干质量比(W/D)评估肺组织的病理学改变；采用ELISA检测支气管肺泡灌洗液中的炎症因子水平和肺组织中髓过氧化物酶(myeloperoxidase

MPO)活性；16S rDNA测序检测肠道菌群的多样性；免疫组织化学染色评估ZO-1和TRPV4的表达。

结果

与LPS组相比，Probiotics组的W/D、炎症因子IL-1β、TNF-α、IL-6水平降低，IL-10升高(

＜0.05)；MPO活性减弱(

＜0.05)；结肠和肺组织中TRPV4表达下调，结肠组织ZO-1表达上调；同时螺杆菌属和脱硫弧菌属的丰度显著改变。

结论

嗜酸乳杆菌能显著减轻LPS诱导的小鼠肺部炎症，可能与肠道内脱硫弧菌属丰度、TRPV4通道活性和肠黏膜屏障通透性有关。

Abstract

Objective

To investigate the effect of

Lactobacillus acidophilus

(

L. acidophilus

) on the inflammation of mice with lipopolysaccharide (LPS)-induced acute pneumonia and the possible mechanism.

Methods

Twenty-one mice were divided into a control group (NC

=6)

a model group (LPS

=8) and a

L. acidophilus

-treated group (Probiotics

=7). The mice in the control group were fed normally

while those in the LPS and Probiotics groups were treated with 10 mg/kg LPS through tracheal drip to establish a mouse model of acute pneumonia

and those in the Probiotics group were given

L. acidophilus

. All of the mice were executed in 7 d after modeling. The pathological changes of lung tissue were assessed by HE staining and wet/dry ratio (W/D) of lung tissue. ELISA was used to detect the levels of inflammatory factors in bronchoalveolar lavage fluid and the activity of myeloperoxidase (MPO) in lung tissue. 16S rDNA sequencing was employed to observe the diversity of intestinal flora

and immunohistochemical (IHC) staining was applied to determine the expression of

ZO-1 and TRPV4.

Results

The Probiotics group had significantly reduced W/D ratio and IL-1β

TNF-α and IL-6 levels

increased IL-10 level (

0.05)

diminished MPO activity (

0.05)

down-regulated TRPV4 expression in colon and lung tissues

and upregulated ZO-1 expression in colon tissue

meanwhile

the abundance of

Helicobacter spp

. and

Desulfovibrio spp

. was significantly altered when compared with the LPS group.

Conclusion

L. acidophilus

alleviates lung inflammation in LPS-induced pneumonia in mice

which may be associated with intestinal abundance of Desulfovibrio spp. in the

activity of TRPV4 channel and intestinal mucosal permeability.

关键词

Keywords

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