scholarly journals Role of preprotachykinin-A gene products on multiple organ injury in LPS-induced endotoxemia

2007 ◽  
Vol 83 (2) ◽  
pp. 288-295 ◽  
Author(s):  
Siaw Wei Ng ◽  
Huili Zhang ◽  
Akhil Hegde ◽  
Madhav Bhatia
Keyword(s):  
Multiple Organ ◽  
Organ Injury ◽  
Gene Products ◽  
Multiple Organ Injury

scholarly journals Ubiquitin-Specific Protease 25 Aggravates Acute Pancreatitis and Acute Pancreatitis-Related Multiple Organ Injury by Destroying Tight Junctions Through Activation of The STAT3 Pathway

2022 ◽  
Vol 9 ◽  
Author(s):  
Zhengru Liu ◽  
Mingming Qi ◽  
Shan Tian ◽  
Qian Yang ◽  
Jian Liu ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Tight Junctions ◽  
Multiple Organ ◽  
Organ Injury ◽  
Pancreatic Acinar Cells ◽  
Stat3 Pathway ◽  
Specific Protease ◽  
Ubiquitin Specific Protease ◽  
Multiple Organ Injury

Ubiquitin-specific protease 25 (USP25) plays an important role in inflammation and immunity. However, the role of USP25 in acute pancreatitis (AP) is still unclear. To evaluate the role of USP25 in AP, we conducted research on clinical AP patients, USP25wild-type(WT)/USP25 knockout (USP25−/−) mice, and pancreatic acinar cells. Our results showed that serum USP25 concentration was higher in AP patients than in healthy controls and was positively correlated with disease severity. AP patients’ serum USP25 levels after treatment were significantly lower than that at the onset of AP. Moreover, USP25 expression was upregulated in cerulein-induced AP in mice, while USP25 deficiency attenuates AP and AP-related multiple organ injury. In vivo and in vitro studies showed that USP25 exacerbates AP by promoting the release of pro-inflammatory factors and destroying tight junctions of the pancreas. We showed that USP25 aggravates AP and AP-related multiple organ injury by activating the signal transducer and activator of transcription 3 (STAT3) pathway. Targeting the action of USP25 may present a potential therapeutic option for treating AP.

The Role of Tumor Necrosis Factor-α (TNF) in Multiple Organ Injury

CHEST Journal ◽  
1989 ◽  
Vol 95 (3) ◽  
pp. 233S-234S
Author(s):  
Robert M. Strieter ◽  
Daniel G. Remick ◽  
Joseph P. Lynch ◽  
Steven L. Kunkel
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Multiple Organ ◽  
Organ Injury ◽  
Factor Α ◽  
Multiple Organ Injury ◽  
Necrosis Factor

scholarly journals The role of PD-L1 in the immune dysfunction that mediates hypoxia-induced multiple organ injury

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Yang Sun ◽  
Jin Tan ◽  
Yuyang Miao ◽  
Qiang Zhang
Keyword(s):  
Immune Regulation ◽  
Therapeutic Potential ◽  
Pathological Condition ◽  
Immune Dysfunction ◽  
Multiple Organ ◽  
Organ Injury ◽  
Cellular Expression ◽  
Obstructive Sleep ◽  
Multiple Organ Injury

AbstractHypoxia is a pathological condition common to many diseases, although multiple organ injuries induced by hypoxia are often overlooked. There is increasing evidence to suggest that the hypoxic environment may activate innate immune cells and suppress adaptive immunity, further stimulating inflammation and inhibiting immunosurveillance. We found that dysfunctional immune regulation may aggravate hypoxia-induced tissue damage and contribute to secondary injury. Among the diverse mechanisms of hypoxia-induced immune dysfunction identified to date, the role of programmed death-ligand 1 (PD-L1) has recently attracted much attention. Besides leading to tumour immune evasion, PD-L1 has also been found to participate in the progression of the immune dysfunction which mediates hypoxia-induced multiple organ injury. In this review, we aimed to summarise the role of immune dysfunction in hypoxia-induced multiple organ injury, the effects of hypoxia on the cellular expression of PD-L1, and the effects of upregulated PD-L1 expression on immune regulation. Furthermore, we summarise the latest information pertaining to the involvement, diagnostic value, and therapeutic potential of immunosuppression induced by PD-L1 in various types of hypoxia-related diseases, including cancers, ischemic stroke, acute kidney injury, and obstructive sleep apnoea.

The selective guanylate cyclase inhibitor ODQ reduces multiple organ injury in rodent models of Gram-positive and Gram-negative shock

2001 ◽  
Vol 29 (8) ◽  
pp. 1599-1608 ◽  
Author(s):  
Kai Zacharowski ◽  
Reinhard Berkels ◽  
Antje Olbrich ◽  
Prabal K. Chatterjee ◽  
Salvatore Cuzzocrea ◽  
...  
Keyword(s):  
Guanylate Cyclase ◽  
Multiple Organ ◽  
Organ Injury ◽  
Rodent Models ◽  
Gram Positive ◽  
Gram Negative ◽  
Multiple Organ Injury ◽  
Negative Shock
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