NLRP3炎症小体在甲型流感病毒H1N1预感染降低小鼠巨噬细胞抗MRSA免疫中的作用

师小函; 石云锋; 巴俊慧; 罗进梅; 胡佳佳; 吴本权

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NLRP3炎症小体在甲型流感病毒H1N1预感染降低小鼠巨噬细胞抗MRSA免疫中的作用

基础研究 | 更新时间：2023-11-01

- NLRP3炎症小体在甲型流感病毒H1N1预感染降低小鼠巨噬细胞抗MRSA免疫中的作用
- Role of NLRP3 Inflammasome in Influenza A Virus H1N1 Attenuates Immunity AgainstSecondary MRSA Infection in Vitro
- 中山大学学报（医学科学版） 2020年41卷第4期页码：542-548
- 作者机构：
  
  中山大学附属第三医院MICU，呼吸与危重症医学科，广东广州 510630
- 作者简介：
  
  师小函，硕士，研究方向：重症及呼吸系统感染性疾病，E-mail: shiningxh@yeah.net
- 基金信息：
  
  广东省科技计划项目(2017A020215177)
- DOI：
  中图分类号： R563.1
- 纸质出版日期：2020-07-15，
  
  收稿日期：2020-01-02，
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师小函,石云锋,巴俊慧等.NLRP3炎症小体在甲型流感病毒H1N1预感染降低小鼠巨噬细胞抗MRSA免疫中的作用[J].中山大学学报（医学科学版）,2020,41(04):542-548.

SHI Xiao-han,SHI Yun-feng,BA Jun-hui,et al.Role of NLRP3 Inflammasome in Influenza A Virus H1N1 Attenuates Immunity AgainstSecondary MRSA Infection in Vitro[J].Journal of Sun Yat-sen University(Medical Sciences),2020,41(04):542-548.
师小函,石云锋,巴俊慧等.NLRP3炎症小体在甲型流感病毒H1N1预感染降低小鼠巨噬细胞抗MRSA免疫中的作用[J].中山大学学报（医学科学版）,2020,41(04):542-548. DOI：

SHI Xiao-han,SHI Yun-feng,BA Jun-hui,et al.Role of NLRP3 Inflammasome in Influenza A Virus H1N1 Attenuates Immunity AgainstSecondary MRSA Infection in Vitro[J].Journal of Sun Yat-sen University(Medical Sciences),2020,41(04):542-548. DOI：

摘要

目的

研究NLRP3炎症小体在经甲型流感病毒H1N1预感染的小鼠巨噬细胞抗耐甲氧西林金黄色葡萄球菌（MRSA）免疫中的活性及作用。

方法

以MRSA分别感染小鼠巨噬细胞（MRSA组）和以甲流病毒H1N1预感染1周的巨噬细胞（H1N1+MRSA组），荧光定量PCR检测各组细胞NLRP3、Caspase-1、IL-1β的mRNA表达强度，免疫荧光及western blot检测细胞中NLRP3的蛋白表达强度，ELISA检测细胞上清液IL-1β的浓度。

结果

MRSA组NLRP3、Caspase-1的mRNA表达水平与空白对照组比无统计学差异（

均

0.05），NLRP3的蛋白表达水平与空白对照组比无统计学差异（

0.05），MRSA组IL-1β的mRNA表达及上清液浓度均明显高于空白对照组（

均

0.01）。H1N1+MRSA组 NLRP3、Caspase-1的mRNA表达水平均高于空白对照组（

均

0.01），NLRP3的蛋白表达水平高于空白对照组（

0.01），上清液IL-1β浓度高于空白对照组（

0.01）。H1N1+MRSA组NLRP3的mRNA表达水平及蛋白表达水平均高于MRSA组（

均

0.01），然而其IL-1β mRNA表达水平低于MRSA组，上清液IL-1β浓度明显低于MRSA组（

0.01）。

结论

MRSA感染肺泡巨噬细胞引起IL-1β的释放不依赖NLRP3炎症小体途径，甲流病毒预感染降低了巨噬细胞抗MRSA免疫IL-1β的表达，该效应可能是甲流病毒感染易继发MRSA肺炎的机制之一。

Abstract

Objective

To explore the role of NLRP3 inflammasome in methicillin-resistant staphylococcus aureus (MRSA) infection secondary to influenza A virus H1N1 (IAV H1N1) in vitro.

Methods

Macrophages RAW264.7 were cultured and then infected with only MRSA for 24 h (MRSA group) and with MRSA for 24 h secondary to H1N1 infection for 1 week in advance (MRSA+H1N1 group)

respectively. Fluorescence quantitative PCR was applied to detect the transcription of NLRP3

Caspase-1 and IL-1β

immunofluorescence and western blot were used to detect NLRP3 protein in cells

and the concentration of IL-1β in supernatant was measured by enzyme linked immunosorbent assay (ELISA).

Results

In MRSA group

the transcriptions of NLRP3 and Caspase-1 mRNA

as well as translation of NLRP3

showed no difference compared with control group

while the expression of IL-1β mRNA and the concentration of IL-1β in supernatant were significantly higher than those in control group (both

0.01). In H1N1+MRSA group

the transcription of NLRP3 and Caspase-1 were significantly higher than those in control group (both

0.01)

the translation of NLRP3 was significantly higher than that in control group (

0.01)

the concentration of IL-1β was significantly higher than that in control group (

0.01). In H1N1+MRSA group

the transcription and translation of NLRP3 were significantly higher than those in MRSA group (both

0.01)

while the transcription of IL-1β was lower than that in MRSA group

and the concentration of IL-1β in supernatant was significantly lower than that in MRSA group (

0.01).

Conclusions

Our study suggests that IL-1β secretion induced by MRSA infection is in a NLRP3 inflammasome independent manner in macrophage. It also suggests that influenza A virus H1N1 infection in advance decreases the release of IL-1β induced by secondary MRSA infection ultimately

which may contribute to the mechanism of MRSA pneumonia secondary to IAV infection.

关键词

NLRP3炎症小体甲型流感病毒H1N1耐甲氧西林金黄色葡萄球菌继发感染

Keywords

NLRP3 Inflammasomeinfluenza A virus H1N1methicillin-resistant staphylococcus aureus (MRSA)secondary infection

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