Respiratory Epithelial Cells Respond to Lactobacillus plantarum but Provide No Cross-Protection against Virus-Induced Inflammation.
Respiratory Epithelial Cells Respond to Lactobacillus plantarum but Provide No Cross-Protection against Virus-Induced Inflammation.
复制标题
呼吸道上皮细胞对植物乳杆菌有反应，但对病毒诱导的炎症没有交叉保护作用。
DOI：
10.3390/v13010002
复制
发表时间：
2020-12-22
期刊：
影响因子：
--
通讯作者：
Rosenberg HF
中科院分区：
文献类型：
--
作者：
Mai E;Percopo CM;Limkar AR;Sek AC;Ma M;Rosenberg HF
病毒诱导的炎症在决定急性呼吸道病毒感染的临床结果中起着关键作用。我们以前已经表明，直接向呼吸道施用免疫生物素植物乳杆菌（Lp）可以防止随后感染小鼠呼吸道病毒病原体的致命炎症反应。虽然脂蛋白介导的保护性反应涉及Toll样受体2（TLR 2）和NOD 2的非冗余贡献，但这些发现的细胞基础仍不清楚。在这里，我们解决了脂蛋白的影响和它的能力，以抑制炎症病毒感染的呼吸道上皮细胞在两个细胞培养模型。我们发现MLE-12细胞和极化小鼠气管上皮细胞（mTEC）对甲型流感病毒感染敏感，并释放促炎细胞因子，包括CCL 2，CCL 5，CXCL 1和CXCL 10，以响应复制病毒。MLE-12细胞表达NOD 2（81 ± 6.3%）和TLR 2（19 ± 4%），对Lp有反应，并且是TLR 2特异性而非NOD 2特异性的生化激动剂。相比之下，我们发现mTEC表达NOD 2（81 ± 17%），但表达最小的TLR 2（0.93 ± 0.58%）;尽管如此，mTEC对Lp和TLR 2激动剂Pam 2CSK 4有反应，但对NOD 2激动剂或双功能TLR 2-NOD 2激动剂CL-429无反应。虽然MLE-12细胞和mTECS都被Lp激活，但通过复制体内有效的实验条件的方案，在响应Lp随后的病毒感染时观察到很少或没有细胞因子抑制。可能需要进一步的研究和更复杂的方法来揭示抑制病毒诱导的炎症反应的关键因素。
Virus-induced inflammation plays a critical role in determining the clinical outcome of an acute respiratory virus infection. We have shown previously that the administration of immunobiotic Lactobacillus plantarum (Lp) directly to the respiratory tract prevents lethal inflammatory responses to subsequent infection with a mouse respiratory virus pathogen. While Lp-mediated protective responses involve non-redundant contributions of both Toll-like receptor 2 (TLR2) and NOD2, the cellular basis of these findings remains unclear. Here, we address the impact of Lp and its capacity to suppress inflammation in virus-infected respiratory epithelial cells in two cell culture models. We found that both MLE-12 cells and polarized mouse tracheal epithelial cells (mTECs) were susceptible to infection with Influenza A and released proinflammatory cytokines, including CCL2, CCL5, CXCL1, and CXCL10, in response to replicating virus. MLE-12 cells express NOD2 (81 ± 6.3%) and TLR2 (19 ± 4%), respond to Lp, and are TLR2-specific, but not NOD2-specific, biochemical agonists. By contrast, we found that mTECs express NOD2 (81 ± 17%) but minimal TLR2 (0.93 ± 0.58%); nonetheless, mTECs respond to Lp and the TLR2 agonist, Pam2CSK4, but not NOD2 agonists or the bifunctional TLR2-NOD2 agonist, CL-429. Although MLE-12 cells and mTECS were both activated by Lp, little to no cytokine suppression was observed in response to Lp followed by virus infection via a protocol that replicated experimental conditions that were effective in vivo. Further study and a more complex approach may be required to reveal critical factors that suppress virus-induced inflammatory responses.
登录
查看更多内容
DOI：
10.1016/j.ijid.2020.10.045
发表时间：
2021-01
期刊：
International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases
影响因子：
--
作者：
Górgolas Hernández-Mora M;Cabello Úbeda A;Prieto-Pérez L;Villar Álvarez F;Álvarez Álvarez B;Rodríguez Nieto MJ;Carrillo Acosta I;Fernández Ormaechea I;Al-Hayani AWM;Carballosa P;Calpena Martínez S;Ezzine F;Castellanos González M;Naya A;López De Las Heras M;Rodríguez Guzmán MJ;Cordero Guijarro A;Broncano Lavado A;Macías Valcayo A;Martín García M;Bécares Martínez J;Fernández Roblas R;Piris Pinilla MÁ;Fortes Alen J;Sánchez Pernaute O;Romero Bueno F;Heili-Frades S;Peces-Barba Romero G
通讯作者：
Peces-Barba Romero G
影响因子：
5.4
作者：
Bonville, CA;Easton, AJ;Domachowske, JB
通讯作者：
Domachowske, JB
DOI：
10.1056/nejmoa0804877
发表时间：
2009-02-05
期刊：
The New England journal of medicine
影响因子：
--
作者：
Hall CB;Weinberg GA;Iwane MK;Blumkin AK;Edwards KM;Staat MA;Auinger P;Griffin MR;Poehling KA;Erdman D;Grijalva CG;Zhu Y;Szilagyi P
通讯作者：
Szilagyi P
影响因子：
5.4
作者：
Hui, Eric Ka-Wai;Smee, Donald F.;Nayak, Debi P.
通讯作者：
Nayak, Debi P.
影响因子：
5.4
作者：
Dyer, Kimberly D.;Drummond, Rebecca A.;Rosenberg, Helene F.
通讯作者：
Rosenberg, Helene F.