scholarly journals CircC3P1 attenuated pro‐inflammatory cytokine production and cell apoptosis in acute lung injury induced by sepsis through modulating miR‐21

2020 ◽  
Vol 24 (19) ◽  
pp. 11221-11229
Author(s):  
Wen‐Yang Jiang ◽  
Jie Ren ◽  
Xing‐Hua Zhang ◽  
Zi‐Long Lu ◽  
Hao‐Jie Feng ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cell Apoptosis ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Cytokine Production

miR-429 regulates alveolar macrophage inflammatory cytokine production and is involved in LPS-induced acute lung injury

2015 ◽  
Vol 471 (2) ◽  
pp. 281-291 ◽  
Author(s):  
Ji Xiao ◽  
Jing Tang ◽  
Quan Chen ◽  
Dan Tang ◽  
Meimei Liu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Alveolar Macrophage ◽  
P38 Mapk ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Cytokine Production

miR-429 targets DUSP1 directly to regulate the activation of p38 MAPK and subsequent production of cytokines in response to LPS stimulation.

scholarly journals Salidroside attenuates acute lung injury via inhibition of inflammatory cytokine production

2021 ◽  
Vol 142 ◽  
pp. 111949
Author(s):  
Dan Song ◽  
Min Zhao ◽  
Liuxiang Feng ◽  
Pingyi Wang ◽  
Yimei Li ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Cytokine Production

scholarly journals Sphingosine 1-phosphate rescues canine LPS-induced acute lung injury and alters systemic inflammatory cytokine production in vivo

2008 ◽  
Vol 152 (5) ◽  
pp. 213-224 ◽  
Author(s):  
William S. Szczepaniak ◽  
Yingze Zhang ◽  
Sarah Hagerty ◽  
Michael T. Crow ◽  
Priya Kesari ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Cytokine Production ◽  
Sphingosine 1 Phosphate

scholarly journals Fusobacterium nucleatum Facilitates Apoptosis, ROS Generation, and Inflammatory Cytokine Production by Activating AKT/MAPK and NF-κB Signaling Pathways in Human Gingival Fibroblasts

2019 ◽  
Vol 2019 ◽  
pp. 1-22 ◽  
Author(s):  
Wenyan Kang ◽  
Zhilong Jia ◽  
Di Tang ◽  
Zhanwei Zhang ◽  
Hui Gao ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Cell Apoptosis ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Fusobacterium Nucleatum ◽  
Human Gingival Fibroblasts ◽  
Ros Generation ◽  
Gingival Fibroblasts ◽  
Inflammatory Cytokine Production ◽  
Pathogenic Effects

Fusobacterium nucleatum (F. nucleatum) plays key roles in the initiation and progression of periodontitis. However, the pathogenic effect of F. nucleatum on human oral tissues and cells has not been fully evaluated. In this study, we aimed to analyze the pathogenic effects of F. nucleatum on human gingival fibroblasts (GFs) and clarify the potential mechanisms. RNA-sequencing analysis confirmed that F. nucleatum significantly altered the gene expression of GF as the stimulation time increased. Cell counting and EdU-labeling assays indicated that F. nucleatum inhibited GF proliferation and promoted cell apoptosis in a time- and dose-dependent manner. In addition, cell apoptosis, intracellular reactive oxygen species (ROS) generation, and proinflammatory cytokine production were dramatically elevated after F. nucleatum stimulation. Furthermore, we found that the AKT/MAPK and NF-κB signaling pathways were significantly activated by F. nucleatum infection and that a large number of genes related to cellular proliferation, apoptosis, ROS, and inflammatory cytokine production downstream of AKT/MAPK and NF-κB signaling pathways were significantly altered in F. nucleatum-stimulated GFs. These findings suggest that F. nucleatum inhibits GF proliferation and promotes cell apoptosis, ROS generation, and inflammatory cytokine production partly by activating the AKT/MAPK and NF-κB signaling pathways. Our study opens a new window for understanding the pathogenic effects of periodontal pathogens on the host oral system.

Sign in / Sign up

Export Citation Format

Share Document