IL-13 induces periostin and eotaxin expression in human primary alveolar epithelial cells: Comparison with paired airway epithelial cells.
IL-13 induces periostin and eotaxin expression in human primary alveolar epithelial cells: Comparison with paired airway epithelial cells.
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DOI：
10.1371/journal.pone.0196256
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发表时间：
2018
期刊：
影响因子：
3.7
通讯作者：
Chu HW
中科院分区：
文献类型：
--
作者：
Ito Y;Al Mubarak R;Roberts N;Correll K;Janssen W;Finigan J;Mishra R;Chu HW
肺泡上皮细胞在肺部炎症和纤维化的发病机制中至关重要，这与2型细胞因子IL-13的过度表达有关。已知IL-13诱导促纤维化（例如，骨膜蛋白）和促炎（例如，在人气道上皮细胞中，IL-13（嗜酸细胞活化趋化因子-3）介导了骨膜蛋白和嗜酸细胞活化趋化因子的表达，但仍不清楚人原代肺泡上皮细胞在IL-13刺激后是否增加骨膜蛋白和嗜酸细胞活化趋化因子的表达。本研究的目的是确定肺泡上皮细胞在IL-13刺激后是否增加骨膜蛋白和嗜酸性粒细胞趋化因子的表达，以及来自相同受试者的肺泡和气道上皮细胞是否对IL-13具有相似的反应。从没有任何肺部疾病的供体中分离成对的肺泡和气道上皮细胞，并在有或没有IL-13的浸没或气-液界面条件下培养。在IL-13刺激的肺泡上皮细胞中观察到骨膜蛋白蛋白和mRNA的上调，这与IL-13刺激的成对气道上皮细胞中的上调相当。IL-13还增加了肺泡上皮细胞中eotaxin-3的表达，但肺泡上皮细胞中eotaxin mRNA的水平低于气道上皮细胞。我们的研究结果表明，人肺泡上皮细胞能够产生骨膜蛋白和嗜酸性粒细胞趋化因子在响应IL-13的刺激。这项研究表明，需要进一步确定肺泡上皮细胞源性介质对肺纤维化的贡献。
Alveolar epithelial cells are critical to the pathogenesis of pulmonary inflammation and fibrosis, which are associated with overexpression of type 2 cytokine IL-13. IL-13 is known to induce the production of profibrotic (e.g., periostin) and pro-inflammatory (e.g., eotaxin-3) mediators in human airway epithelial cells, but it remains unclear if human primary alveolar epithelial cells increase periostin and eotaxin expression following IL-13 stimulation. The goals of this study are to determine if alveolar epithelial cells increase periostin and eotaxin expression upon IL-13 stimulation, and if alveolar and airway epithelial cells from the same subjects have similar responses to IL-13. Paired alveolar and airway epithelial cells were isolated from donors without any lung disease, and cultured under submerged or air-liquid interface conditions with or without IL-13. Up-regulation of periostin protein and mRNA was observed in IL-13-stimulated alveolar epithelial cells, which was comparable to that in IL-13-stimulated paired airway epithelial cells. IL-13 also increased eotaxin-3 expression in alveolar epithelial cells, but the level of eotaxin mRNA was lower in alveolar epithelial cells than in airway epithelial cells. Our findings demonstrate that human alveolar epithelial cells are able to produce periostin and eotaxin in responses to IL-13 stimulation. This study suggests the need to further determine the contribution of alveolar epithelial cell-derived mediators to pulmonary fibrosis.
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影响因子：
3.7
作者：
Ohta S;Okamoto M;Fujimoto K;Sakamoto N;Takahashi K;Yamamoto H;Kushima H;Ishii H;Akasaka K;Ono J;Kamei A;Azuma Y;Matsumoto H;Yamaguchi Y;Aihara M;Johkoh T;Kawaguchi A;Ichiki M;Sagara H;Kadota JI;Hanaoka M;Hayashi SI;Kohno S;Hoshino T;Izuhara K;Consortium for Development of Diagnostics for Pulmonary Fibrosis Patients (CoDD-PF)
通讯作者：
Consortium for Development of Diagnostics for Pulmonary Fibrosis Patients (CoDD-PF)
影响因子：
5.8
作者：
Keating, Dominic T.;Sadlier, Denise M.;Patricelli, Andrea;Smith, Sinead M.;Walls, Dermot;Egan, Jim J.;Doran, Peter P.
通讯作者：
Doran, Peter P.
DOI：
10.1016/j.jaci.2011.10.043
发表时间：
2012-03
期刊：
The Journal of allergy and clinical immunology
影响因子：
--
作者：
Wu Q;Jiang D;Smith S;Thaikoottathil J;Martin RJ;Bowler RP;Chu HW
通讯作者：
Chu HW
影响因子：
6.9
作者：
Suzaki, Isao;Kawano, Shuichi;Rubin, Bruce K.
通讯作者：
Rubin, Bruce K.
影响因子：
6.7
作者：
Birring, SS;Parker, D;Bradding, P
通讯作者：
Bradding, P