Vimentin affects inflammation and neutrophil recruitment in airway epithelium during Streptococcus suis serotype 2 infection.
Vimentin affects inflammation and neutrophil recruitment in airway epithelium during Streptococcus suis serotype 2 infection.
复制标题
波形蛋白影响猪链球菌血清型 2 感染期间气道上皮的炎症和中性粒细胞募集
DOI：
10.1186/s13567-023-01135-3
复制
发表时间：
2023-01-30
影响因子：
4.4
通讯作者：
中科院分区：
文献类型：
--
作者：
猪链球菌血清型 2 (SS2) 经常定植于猪的上呼吸道，可引起猪链球菌病，临床表现为肺炎、脑膜炎和败血症。此前，我们已经证明波形蛋白（一种中间丝蛋白）参与SS2穿过气管上皮屏障的过程。侵袭性疾病的发生与SS2引起的过度局部炎症密切相关；然而，波形蛋白在气道上皮炎症中的作用仍不清楚。在这里，我们发现波形蛋白缺陷小鼠表现出肺损伤减轻，促炎细胞因子白细胞介素-6 (IL-6)、肿瘤坏死因子-α (TNF-α) 和 IL-8 同源物角质形成细胞衍生趋化因子 (KC) 的产生减少，并且鼻内感染 SS2 后肺部中性粒细胞显着减少。我们还发现，没有波形蛋白的猪气管上皮细胞 (STEC) 显示 IL-6、TNF-α 和 IL-8 的转录减少。 SS2 感染导致 STEC 中波形蛋白的重新组装，波形蛋白丝的药理学破坏阻止了这些促炎细胞因子的转录。此外，波形蛋白的缺乏无法增加核苷酸寡聚结构域蛋白 2 (NOD2) 的转录（已知该蛋白与波形蛋白相互作用）以及 NF-κB 蛋白 p65 的磷酸化。这项研究提供了关于波形蛋白如何促进过度气道炎症，从而加剧气道损伤和 SS2 诱导的全身感染的见解。在线版本包含可在 10.1186/s13567-023-01135-3 获取的补充材料。
Streptococcus suis serotype 2 (SS2) frequently colonizes the swine upper respiratory tract and can cause Streptococcal disease in swine with clinical manifestations of pneumonia, meningitis, and septicemia. Previously, we have shown that vimentin, a kind of intermediate filament protein, is involved in the penetration of SS2 through the tracheal epithelial barrier. The initiation of invasive disease is closely related to SS2-induced excessive local inflammation; however, the role of vimentin in airway epithelial inflammation remains unclear. Here, we show that vimentin deficient mice exhibit attenuated lung injury, diminished production of proinflammatory cytokines interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and the IL-8 homolog, keratinocyte-derived chemokine (KC), and substantially reduced neutrophils in the lungs following intranasal infection with SS2. We also found that swine tracheal epithelial cells (STEC) without vimentin show decreased transcription of IL-6, TNF-α, and IL-8. SS2 infection caused reassembly of vimentin in STEC, and pharmacological disruption of vimentin filaments prevented the transcription of those proinflammatory cytokines. Furthermore, deficiency of vimentin failed to increase the transcription of nucleotide oligomerization domain protein 2 (NOD2), which is known to interact with vimentin, and the phosphorylation of NF-κB protein p65. This study provides insights into how vimentin promotes excessive airway inflammation, thereby exacerbating airway injury and SS2-induced systemic infection. The online version contains supplementary material available at 10.1186/s13567-023-01135-3.
登录
查看更多内容
影响因子：
12.4
作者：
Jang HR;Shin SB;Kim CH;Won JY;Xu R;Kim DE;Yim H
通讯作者：
Yim H
影响因子：
3.3
作者：
Li, Wei;Wan, Yun;Zhou, Rui
通讯作者：
Zhou, Rui
DOI：
10.1073/pnas.2113874119
发表时间：
2022-02-08
影响因子：
11.1
作者：
Amraei R;Xia C;Olejnik J;White MR;Napoleon MA;Lotfollahzadeh S;Hauser BM;Schmidt AG;Chitalia V;Mühlberger E;Costello CE;Rahimi N
通讯作者：
Rahimi N
DOI：
10.1007/s00018-020-03656-y
发表时间：
2021-03
期刊：
Cellular and molecular life sciences : CMLS
影响因子：
--
作者：
Ciesielska A;Matyjek M;Kwiatkowska K
通讯作者：
Kwiatkowska K
影响因子：
13.2
作者：
Goyette-Desjardins, Guillaume;Auger, Jean-Philippe;Xu, Jianguo;Segura, Mariela;Gottschalk, Marcelo
通讯作者：
Gottschalk, Marcelo