Ionizing radiation promotes CCL27 secretion from keratinocytes through the cross talk between TNF-α and ROS

2016 ◽  
Vol 31 (3) ◽  
pp. e21868 ◽  
Author(s):  
Qian Zhang ◽  
Linlin Zhu ◽  
Gang Wang ◽  
Ye Zhao ◽  
Na Xiong ◽  
...  
2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Yasmen F. Mahran ◽  
Amira M. Badr ◽  
Alhanouf Aldosari ◽  
Raghad Bin-Zaid ◽  
Hind N. Alotaibi

Premature ovarian failure (POF) is a common cause of infertility in premenopausal women who are unavoidably exposed to cytotoxic therapy. Radiotherapy is one of the most effective cytotoxic treatments. However, the radiosensitivity of ovarian tissues limits its therapeutic outcome and results in the depletion of the primordial follicle and loss of fertility. Therefore, the need for an effective radioprotective therapy is evident especially when none of the current clinically used modalities for radioprotection succeeds efficiently. The present study investigated the potential radioprotective effect of carvacrol (CAR) (80 mg) or thymol (80 mg) on gamma- (γ-) irradiation-induced ovarian damage as well as their role in the cross-talk between IGF-1 and TNF-α signaling and antioxidative activity. In immature female Wister rats, a single dose of whole-body irradiation (3.2 Gy, L D 20 ) produced considerable ovarian damage, which was evident by histopathological findings and hormonal changes. Interestingly, pretreatment with CAR or thymol significantly enhanced the follicular development and restored the anti-Mullerian hormone (AMH), E2, and FSH levels. Both essential oils improved the irradiation-mediated oxidative stress and reduction in proliferating cell nuclear antigen (PCNA) expression. Moreover, irradiated rats exhibited an inverse relationship between IGF-1 and TNF-α levels two days post irradiation, which was further inverted by the pretreatment with CAR and thymol and ought to contribute in their radioprotective mechanisms. In conclusion, CAR and thymol showed a radioprotective effect and rescued the ovarian reserve mainly through counteracting oxidative stress and the dysregulated cross-talk between IGF-1 and TNF-α.


2012 ◽  
Vol 393 (1-2) ◽  
pp. 101-106 ◽  
Author(s):  
Vijaya Lakshmi Simhadri ◽  
Hinrich P. Hansen ◽  
Venkateswara R. Simhadri ◽  
Katrin S. Reiners ◽  
Martina Bessler ◽  
...  

Abstract The interplay between dendritic cells (DCs) and natural killer (NK) cells directs adaptive immune responses. The molecular basis of the cross-talk is largely undefined. Here, we provide evidence for a contribution of CD30 (TNFRSF8) and its ligand CD30L (TNFSF8) expressed on NK cells and DCs, respectively. We demonstrate that CD30-mediated engagement of CD30L induced cytokine secretion from immature DCs via the mitogen-activated protein kinase pathway. Moreover, CD30L engagement promoted differentiation to mature DCs. On the contrary, the engagement of CD30 on NK cells resulted in an NF-κB-dependent release of TNF-α/IFN-γ. These data uncover a novel and unexpected role for CD30/CD30L that contributes to proinflammatory immune responses.


2019 ◽  
Vol 20 (9) ◽  
pp. 2346 ◽  
Author(s):  
Delvac Oceandy ◽  
Bella Amanda ◽  
Faisal Ashari ◽  
Zakiyatul Faizah ◽  
M Aziz ◽  
...  

The regulation of cell death through apoptosis is essential to a number of physiological processes. Defective apoptosis regulation is associated with many abnormalities including anomalies in organ development, altered immune response and the development of cancer. Several signalling pathways are known to regulate apoptosis including the Tumour Necrosis Factor-α (TNF-α) and Hippo signalling pathways. In this paper we review the cross-talk between the TNF-α pathway and the Hippo signalling pathway. Several molecules that tightly regulate the Hippo pathway, such as members of the Ras-association domain family member (RASSF) family proteins, interact and modulate some key proteins within the TNF-α pathway. Meanwhile, TNF-α stimulation also affects the expression and activation of core components of the Hippo pathway. This implies the crucial role of signal integration between these two major pathways in regulating apoptosis.


2018 ◽  
Vol 18 (18) ◽  
pp. 1567-1571
Author(s):  
Anna Lucia Tornesello ◽  
Luigi Buonaguro ◽  
Maria Lina Tornesello ◽  
Franco M. Buonaguro

2017 ◽  
Vol 33 (3) ◽  
pp. 315-324 ◽  
Author(s):  
Chang Liu ◽  
Dong-Ying Yan ◽  
Xuan Tan ◽  
Zhuo Ma ◽  
Can Wang ◽  
...  

2021 ◽  
Vol 1 (1) ◽  
pp. 55-63
Author(s):  
NingJie Hao ◽  
Xiaoxiao Zou ◽  
Xiaoxia Lin ◽  
Ruqiong Cai ◽  
Wenjun Xiao ◽  
...  

Rheumatology ◽  
2021 ◽  
Author(s):  
Sicília Rezende Oliveira ◽  
José Alcides A de Arruda ◽  
Ayda Henriques Schneider ◽  
Valessa Florindo Carvalho ◽  
Caio Machado ◽  
...  

Abstract Objectives Neutrophil extracellular traps (NETs) play a role in the pathogenesis of periodontitis and rheumatoid arthritis (RA). However, it remains poorly understood whether NETs participate in the cross-talk between periodontitis and RA. Herein, we investigated the production of NETs in individuals with periodontitis and RA and its association with clinical parameters. The impact of periodontal therapy on RA and NET release was also assessed. Methods The concentration of NETs and cytokines was determined in the saliva and plasma of individuals with early RA (n = 24), established RA (n = 64), and individuals without RA (n = 76). The influence of periodontitis on the production of NETs and cytokines was also evaluated. Results Individuals with early RA had a higher concentration of NETs in saliva and plasma than individuals with established RA or without RA. Periodontitis resulted in an increase in the concentration of NETs of groups of individuals without RA and with early RA. The proportion of individuals with high concentrations of IL-6, IL-10 and GM-CSF was higher among individuals with periodontitis than among individuals without periodontitis. The concentrations of TNF-α, IL-6, IL-17/IL-25, and IL-28A were particularly high in individuals with early RA. Worse periodontal clinical parameters, RA onset and RA activity were significantly associated with circulating NETs. Periodontal therapy was associated with a reduction in the concentration of NETs and inflammatory cytokines and amelioration in periodontitis and RA. Conclusion This study reveals that NETs are a possible link between periodontitis and RA, with periodontal therapy resulting in a dramatic switch in circulating NET levels.


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