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Neutrophil-Mediated Lung Injury Both via TLR2-Dependent Production of IL-1α and IL-12 p40, and TLR2-Independent CARDS Toxin after Mycoplasma pneumoniae Infection in Mice.肺炎支原体感染小鼠中性粒细胞通过 TLR2 依赖性产生 IL-1α 和 IL-12 p40 以及 TLR2 非依赖性 CARDS 毒素导致肺损伤。
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本文引用的文献

1
A Non-Human Primate Model of Severe Pneumococcal Pneumonia.重症肺炎球菌肺炎的非人灵长类动物模型
PLoS One. 2016 Nov 17;11(11):e0166092. doi: 10.1371/journal.pone.0166092. eCollection 2016.
2
Incident asthma and Mycoplasma pneumoniae: A nationwide cohort study.事件性哮喘与肺炎支原体:一项全国性队列研究。
J Allergy Clin Immunol. 2016 Apr;137(4):1017-1023.e6. doi: 10.1016/j.jaci.2015.09.032. Epub 2015 Nov 14.
3
Macrolides for chronic asthma.用于慢性哮喘的大环内酯类药物。
Cochrane Database Syst Rev. 2015 Sep 15(9):CD002997. doi: 10.1002/14651858.CD002997.pub4.
4
Changes in levels of IL-9, IL-17, IFN-γ, dendritic cell numbers and TLR expression in peripheral blood in asthmatic children with Mycoplasma pneumoniae infection.支原体肺炎感染的哮喘儿童外周血中白细胞介素-9、白细胞介素-17、干扰素-γ水平、树突状细胞数量及Toll样受体表达的变化
Int J Clin Exp Pathol. 2015 May 1;8(5):5263-72. eCollection 2015.
5
Changes of serum TNF-α, IL-5 and IgE levels in the patients of mycoplasma pneumonia infection with or without bronchial asthma.支原体肺炎感染合并或不合并支气管哮喘患者血清肿瘤坏死因子-α、白细胞介素-5和免疫球蛋白E水平的变化
Int J Clin Exp Med. 2015 Mar 15;8(3):3901-6. eCollection 2015.
6
Mycoplasma pneumoniae CARDS toxin exacerbates ovalbumin-induced asthma-like inflammation in BALB/c mice.肺炎支原体CARDS毒素加剧卵清蛋白诱导的BALB/c小鼠哮喘样炎症。
PLoS One. 2014 Jul 24;9(7):e102613. doi: 10.1371/journal.pone.0102613. eCollection 2014.
7
Mycoplasma pneumoniae CARDS toxin is internalized via clathrin-mediated endocytosis.肺炎支原体 CARDS 毒素通过网格蛋白介导的内吞作用内化。
PLoS One. 2013 May 7;8(5):e62706. doi: 10.1371/journal.pone.0062706. Print 2013.
8
Mycoplasma pneumoniae in children with acute and refractory asthma.肺炎支原体与儿童急性难治性哮喘
Ann Allergy Asthma Immunol. 2013 May;110(5):328-334.e1. doi: 10.1016/j.anai.2013.01.022. Epub 2013 Feb 23.
9
Mycoplasma pneumoniae CARDS toxin induces pulmonary eosinophilic and lymphocytic inflammation.肺炎支原体 CARDS 毒素诱导肺嗜酸性粒细胞和淋巴细胞炎症。
Am J Respir Cell Mol Biol. 2012 Jun;46(6):815-22. doi: 10.1165/rcmb.2011-0135OC. Epub 2012 Jan 26.
10
Bronchoconstriction in nonhuman primates: a species comparison.非人类灵长类动物的支气管收缩:种属比较。
J Appl Physiol (1985). 2011 Sep;111(3):791-8. doi: 10.1152/japplphysiol.00162.2011. Epub 2011 Jun 23.

肺炎支原体与社区获得性呼吸窘迫综合征毒素的免疫病理效应。灵长类动物模型。

The Immunopathologic Effects of Mycoplasma pneumoniae and Community-acquired Respiratory Distress Syndrome Toxin. A Primate Model.

作者信息

Maselli Diego J, Medina Jorge L, Brooks Edward G, Coalson Jacqueline J, Kannan Thirumalai R, Winter Vicki T, Principe Molly, Cagle Marianna P, Baseman Joel B, Dube Peter H, Peters Jay I

机构信息

1 Division of Pulmonary Diseases and Critical Care Medicine, Department of Medicine.

2 Department of Microbiology and Immunology.

出版信息

Am J Respir Cell Mol Biol. 2018 Feb;58(2):253-260. doi: 10.1165/rcmb.2017-0006OC.

DOI:10.1165/rcmb.2017-0006OC
PMID:28915064
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5805996/
Abstract

Mycoplasma pneumoniae infection has been linked to poor asthma outcomes. M. pneumoniae produces an ADP-ribosylating and vacuolating toxin called community-acquired respiratory distress syndrome (CARDS) toxin that has a major role in inflammation and airway dysfunction. The objective was to evaluate the immunopathological effects in primates exposed to M. pneumoniae or CARDS toxin. A total of 13 baboons were exposed to M. pneumoniae or CARDS toxin. At Days 7 and 14, BAL fluid was collected and analyzed for cell count, percent of each type of cell, CARDS toxin by PCR, CARDS toxin by antigen capture, eosinophilic cationic protein, and cytokine profiles. Serum IgM, IgG, and IgE responses to CARDS toxin were measured. All animals had a necropsy for analysis of the histopathological changes on lungs. No animal developed signs of infection. The serological responses to CARDS toxin were variable. At Day 14, four of seven animals exposed to M. pneumoniae and all four animals exposed to CARDS toxin developed histological "asthma-like" changes. T cell intracellular cytokine analysis revealed an increasing ratio of IL-4/IFN-γ over time. Both M. pneumoniae and CARDS toxin exposure resulted in similar histopathological pulmonary changes, suggesting that CARDS toxin plays a major role in the inflammatory response.

摘要

肺炎支原体感染与哮喘不良预后有关。肺炎支原体产生一种名为社区获得性呼吸窘迫综合征(CARDS)毒素的ADP核糖基化和空泡化毒素,该毒素在炎症和气道功能障碍中起主要作用。目的是评估暴露于肺炎支原体或CARDS毒素的灵长类动物的免疫病理效应。总共13只狒狒暴露于肺炎支原体或CARDS毒素。在第7天和第14天,收集支气管肺泡灌洗(BAL)液并分析细胞计数、每种细胞类型的百分比、通过聚合酶链反应(PCR)检测的CARDS毒素、通过抗原捕获检测的CARDS毒素、嗜酸性阳离子蛋白和细胞因子谱。检测血清对CARDS毒素的IgM、IgG和IgE反应。所有动物均进行尸检以分析肺部的组织病理学变化。没有动物出现感染迹象。对CARDS毒素的血清学反应各不相同。在第14天,七只暴露于肺炎支原体的动物中有四只以及所有四只暴露于CARDS毒素的动物出现了组织学上的“哮喘样”变化。T细胞细胞内细胞因子分析显示,随着时间的推移,IL-4/IFN-γ的比例增加。暴露于肺炎支原体和CARDS毒素均导致类似的肺部组织病理学变化,这表明CARDS毒素在炎症反应中起主要作用。