Airway and parenchyma immune cells in influenza A(H1N1)pdm09 viral and non-viral diffuse alveolar damage.
Airway and parenchyma immune cells in influenza A(H1N1)pdm09 viral and non-viral diffuse alveolar damage.
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DOI：
10.1186/s12931-017-0630-x
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发表时间：
2017-08-03
影响因子：
5.8
通讯作者：
Mauad T
中科院分区：
文献类型：
--
作者：
Buttignol M;Pires-Neto RC;Rossi E Silva RC;Albino MB;Dolhnikoff M;Mauad T
弥漫性肺泡损伤（DAD）是急性呼吸窘迫综合征（ARDS）的组织学替代物，具有多因素病因。因此，不同表现的DAD的免疫病理可能不同。本研究的目的是比较尸检DAD病例中病毒性（甲型H1N1流感）pdm09与非病毒性肺外病因的肺免疫病理学。44例患者肺组织分为H1N1组（n = 15），表现为甲型H1N1流感pdm09感染引起的严重肺损伤；ARDS组（n = 13），以非肺源性DAD患者为特征；对照组（n = 16），由非肺部原因死亡的患者组成。免疫组织化学和图像分析用于量化实质和小气道中的几种免疫细胞标记物。两组肺实质及小气道内嗜中性粒细胞及巨噬细胞表达均升高。而H1N1组肺实质中CD4+、CD8+ T淋巴细胞、CD83+树突状细胞、颗粒酶a +和自然杀伤细胞密度的表达均高于对照组（p < 0.05）。在小气道中，两组胰蛋白酶+肥大细胞和树突状+细胞的细胞密度均降低，IL-17水平升高（p < 0.05）。甲型H1N1病毒pdm09引起的DAD与细胞毒性炎症表型相关，在相对于小气道的实质中有部分不同的反应。在非病毒性DAD中，主要免疫细胞改变发生在小气道水平，加强了小气道在DAD渗出期发病机制中的作用。本文的在线版本（doi:10.1186/s12931-017-0630-x）包含补充材料，可供授权用户使用。
Diffuse alveolar damage (DAD), which is the histological surrogate for acute respiratory distress syndrome (ARDS), has a multifactorial aetiology. Therefore it is possible that the immunopathology differs among the various presentations of DAD. The aim of this study is to compare lung immunopathology of viral (influenza A(H1N1)pdm09) to non-viral, extrapulmonary aetiologies in autopsy cases with DAD. The lung tissue of 44 patients, was divided in the H1N1 group (n = 15) characterized by severe pulmonary injury due to influenza A(H1N1)pdm09 infection; the ARDS group (n = 13), characterized by patients with DAD due to non-pulmonary causes; and the Control group (n = 16), consisting of patients with non-pulmonary causes of death. Immunohistochemistry and image analysis were used to quantify, in the parenchyma and small airways, several immune cell markers. Both DAD groups had higher expression of neutrophils and macrophages in parenchyma and small airways. However, there was a higher expression of CD4+ and CD8+ T lymphocytes, CD83+ dendritic cells, granzyme A+ and natural killer + cell density in the lung parenchyma of the H1N1 group (p < 0.05). In the small airways, there was a lower cell density of tryptase + mast cells and dendritic + cells and an increase of IL-17 in both DAD groups (p < 0.05). DAD due to viral A(H1N1)pdm09 is associated with a cytotoxic inflammatory phenotype, with partially divergent responses in the parenchyma relative to the small airways. In non-viral DAD, main immune cell alterations were found at the small airway level, reinforcing the role of the small airways in the pathogenesis of the exudative phase of DAD. The online version of this article (doi:10.1186/s12931-017-0630-x) contains supplementary material, which is available to authorized users.
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DOI：
10.1164/rccm.201410-1782oc
发表时间：
2016-02-15
影响因子：
24.7
作者：
Muir, Roshell;Osbourn, Megan;Ingram, Rebecca J.
通讯作者：
Ingram, Rebecca J.
影响因子：
15.1
作者：
Morales, Maina M. B.;Pires-Neto, Ruy C.;Dolhnikoff, Marisa
通讯作者：
Dolhnikoff, Marisa
DOI：
10.1186/cc8208
发表时间：
2009
期刊：
Critical care (London, England)
影响因子：
--
作者：
Bermejo-Martin JF;Ortiz de Lejarazu R;Pumarola T;Rello J;Almansa R;Ramírez P;Martin-Loeches I;Varillas D;Gallegos MC;Serón C;Micheloud D;Gomez JM;Tenorio-Abreu A;Ramos MJ;Molina ML;Huidobro S;Sanchez E;Gordón M;Fernández V;Del Castillo A;Marcos MA;Villanueva B;López CJ;Rodríguez-Domínguez M;Galan JC;Cantón R;Lietor A;Rojo S;Eiros JM;Hinojosa C;Gonzalez I;Torner N;Banner D;Leon A;Cuesta P;Rowe T;Kelvin DJ
通讯作者：
Kelvin DJ
DOI：
10.4049/jimmunol.0900995
发表时间：
2009-10-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Crowe CR;Chen K;Pociask DA;Alcorn JF;Krivich C;Enelow RI;Ross TM;Witztum JL;Kolls JK
通讯作者：
Kolls JK
影响因子：
9.6
作者：
Parambil, Joseph G.;Myers, Jeffrey L.;Ryu, Jay H.
通讯作者：
Ryu, Jay H.