Streptococcus pyogenes induces epithelial inflammatory responses through NF-κB/MAPK signaling pathways

2006 ◽  
Vol 8 (6) ◽  
pp. 1440-1449 ◽  
Author(s):  
Pei-Jane Tsai ◽  
Ying-Huei Chen ◽  
Chieh-Hsing Hsueh ◽  
Hsiao-Chun Hsieh ◽  
Ya-Hui Liu ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Streptococcus Pyogenes ◽  
Inflammatory Responses ◽  
Mapk Signaling ◽  
Mapk Signaling Pathways

Autophagy mediates avian influenza H5N1 pseudotyped particle-induced lung inflammation through NF-κB and p38 MAPK signaling pathways

2014 ◽  
Vol 306 (2) ◽  
pp. L183-L195 ◽  
Author(s):  
Hong Pan ◽  
Yijuan Zhang ◽  
Zichao Luo ◽  
Ping Li ◽  
Lanlan Liu ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Lung Inflammation ◽  
H5n1 Virus ◽  
Inflammatory Responses ◽  
Mapk Signaling ◽  
Lung Epithelial Cells ◽  
Mapk Signaling Pathways

Since avian influenza virus H5N1-induced hypercytokemia plays a key role in acute lung injury, understanding its molecular mechanism is highly desirable for discovering therapeutic targets against H5N1 infection. In the present study, we investigated the role of autophagy in H5N1-induced lung inflammation by using H5N1 pseudotyped viral particles (H5N1pps). The results showed that H5N1pps significantly induced autophagy both in A549 human lung epithelial cells and in mouse lung tissues, which was primarily due to hemagglutinin (HA) of H5N1 virus. Blocking autophagy with 3-methyladenine (an autophagy inhibitor) or siRNA knockdown of autophagy-related genes ( beclin1 and atg5) dramatically attenuated H5N1pp-induced proinflammatory cytokines and chemokines, such as IL-1β, TNF-α, IL-6, CCL2, and CCL5, both in vitro and in vivo. Autophagy-mediated inflammatory responses involved the activation of NF-κB and p38 MAPK signaling pathways, which required the presence of clathrin but did not rely on p62 or autophagosome-lysosome fusion. On the other hand, the activation of NF-κB also promoted H5N1pp-induced autophagosome formation. These data indicated a positive feedback loop between autophagy and NF-κB signaling cascade, which could exacerbate H5N1pp-induced lung inflammation. Our data demonstrated an essential role of autophagy in H5N1pp-triggered inflammatory responses, and targeting the autophagic pathway could be a promising strategy to treat H5N1 virus-caused lung inflammation.

scholarly journals Activation of the NF-κB and MAPK Signaling Pathways Contributes to the Inflammatory Responses, but Not Cell Injury, in IPEC-1 Cells Challenged with Hydrogen Peroxide

2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Kan Xiao ◽  
Congcong Liu ◽  
Zhixiao Tu ◽  
Qiao Xu ◽  
Shaokui Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Signaling Pathways ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Mapk Signaling ◽  
Intestinal Cell ◽  
Ldh Activity ◽  
Junction Protein ◽  
Mapk Signaling Pathways

Oxidative stress can lead to intestinal cell injury as well as the induction of inflammation. It is not clear whether inflammation is an important factor leading to cell injury caused by oxidative stress. The purpose of this study was to investigate the role of inflammation in intestinal injury caused by hydrogen peroxide (H2O2). Our results revealed that H2O2 stimulation significantly decreased the viability of intestinal porcine epithelial cells (IPEC-1), increased lactate dehydrogenase (LDH) activity, and disrupted the distribution of the tight junction protein claudin-1. H2O2 significantly increased the mRNA expression of interleukin-6 (IL-6), IL-8, and tumor necrosis factor-α (TNF-α). H2O2 stimulation also led to increased phosphorylation of p38 and jun N-terminal kinase (JNK), and p65 NF-κB protein translocation into the nucleus of IPEC-1 cells. Cells treated with the NF-κB inhibitor (BAY11-7082), the p38 inhibitor (SB202190), or the JNK inhibitor (PD98059) significantly decreased mRNA and protein expression of IL-6, IL-8, and TNF-α. However, treatment with mitogen-activated protein kinase (MAPK) or NF-κB inhibitors did not prevent the damage effect on cell viability, LDH activity, or the distribution of claudin-1 in cells challenged with H2O2. In summary, our data demonstrate that activation of the NF-κB and MAPK signaling pathways can contribute to the inflammatory response, but not cell injury, in IPEC-1 cells challenged with H2O2.

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