Endoplasmic reticulum stress of Kupffer cells involved in the conversion of natural regulatory T cells to Th17 cells in liver ischemia‐reperfusion injury

Gao, Jialin; Jiang, Zhonghua; Wang, Shuai; Zhou, Yuan; Shi, Xiaolei; Feng, Min

doi:10.1111/jgh.13163

Cited by 25 publications

(24 citation statements)

References 26 publications

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“…In addition, AKI leads to increased levels of systemic IL-6 in rats, which activates Kupffer cells to produce IL-10 in the liver. 93 In contrast, mice treated with neutralizing antibodies against IL-17A, TNF-α or IL-6 or mice deficient in IL-17A receptor, TNF-α or IL-6 seem to be protected against hepatic and intestine injury. 90 In addition, oxidative stress (ie, decreased hepatic superoxide dismutase and catalase activity, as well as increased levels of hepatic malondialdehyde and protein carbonyl) accompanied by decreased glutathione levels (an important protective endogenous free radical scavenger) in the liver has been described in mouse 90 and rat 91 models of renal ischaemia-reperfusion injury.…”

Section: Aki and Liver/intestine Dysfunctionmentioning

confidence: 98%

“…89 Of note, an increased IL-17A expression in mouse models of liver ischaemia-reperfusion has been consistently associated with an unbalanced CD4 + T helper cell 17/T regulatory cell response. 93 In contrast, mice treated with neutralizing antibodies against IL-17A, TNF-α or IL-6 or mice deficient in IL-17A receptor, TNF-α or IL-6 seem to be protected against hepatic and intestine injury. 89…”

Section: Aki and Liver/intestine Dysfunctionmentioning

confidence: 98%

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Distant organ dysfunction in acute kidney injury

2019

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Acute kidney injury (AKI) is a common complication in critically ill patients and it is associated with increased morbidity and mortality. Epidemiological and clinical data show that AKI is linked to a wide range of distant organ injuries, with the lungs, heart, liver, and intestines representing the most clinically relevant affected organs. This distant organ injury during AKI predisposes patients to progression to multiple organ dysfunction syndrome and ultimately, death. The strongest direct evidence of distant organ injury occurring in AKI has been obtained from animal models. The identified mechanisms include systemic inflammatory changes, oxidative stress, increases in leucocyte trafficking and the activation of proapoptotic pathways.Understanding the pathways driving AKI-induced distal organ injury are critical for the development and refinement of therapies for the prevention and attenuation of AKI-related morbidity and mortality. The purpose of this review is to summarize both clinical and preclinical studies of AKI and its role in distant organ injury.

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Section: Aki and Liver/intestine Dysfunctionmentioning

confidence: 98%

Section: Aki and Liver/intestine Dysfunctionmentioning

confidence: 98%

Distant organ dysfunction in acute kidney injury

2019

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“…The role of the DNA damage response in this scenario may represent a consequence of the loss of redox buffers (110,111,178,298,390,404,574,591,705,717), and the loss of NADPH abundance may decrease the threshold for several pathways of regulated necrosis, including necroptosis and ferroptosis, in this setting (280,384,385,738). As cellular demise is regulated by ER stress (106,184,248,306,329,389,634,674,738) in a balancing act with autophagy (8,77,280,363,369,379,425,430,523,623,631,686), the complexity of the regulation of necrosis during transplantation becomes obvious. However, it will be required to unreveal this system in a much more complete manner to therapeutically optimize the inevitable sensitization to acute allograft rejection and antibody-mediated rejection (see below).…”

Section: Ischemia-reperfusion Injury and The Redox Systemmentioning

confidence: 99%

Origin and Consequences of Necroinflammation

Sarhan

Land

Tonnus

et al. 2018

Physiological Reviews

165

152

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When cells undergo necrotic cell death in either physiological or pathophysiological settings in vivo, they release highly immunogenic intracellular molecules and organelles into the interstitium and thereby represent the strongest known trigger of the immune system. With our increasing understanding of necrosis as a regulated and genetically determined process (RN, regulated necrosis), necrosis and necroinflammation can be pharmacologically prevented. This review discusses our current knowledge about signaling pathways of necrotic cell death as the origin of necroinflammation. Multiple pathways of RN such as necroptosis, ferroptosis, and pyroptosis have been evolutionary conserved most likely because of their differences in immunogenicity. As the consequence of necrosis, however, all necrotic cells release damage associated molecular patterns (DAMPs) that have been extensively investigated over the last two decades. Analysis of necroinflammation allows characterizing specific signatures for each particular pathway of cell death. While all RN-pathways share the release of DAMPs in general, most of them actively regulate the immune system by the additional expression and/or maturation of either pro- or anti-inflammatory cytokines/chemokines. In addition, DAMPs have been demonstrated to modulate the process of regeneration. For the purpose of better understanding of necroinflammation, we introduce a novel classification of DAMPs in this review to help detect the relative contribution of each RN-pathway to certain physiological and pathophysiological conditions.

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“…Since these topics have recently taken center stage in the research field of stress responses → RCD → immunity, they will be detailed below. In particular, the impact of IRI on necroptosis, parthanatos, and (more pronounced) ferroptosis , ER stress/UPR , ER stress/UPR/autophagy , and DDR has recently been highlighted. These reports clearly attest IRI to be critically implicated in the emission of a plethora of DAMPs inherently capable—via recognition by PRRs on/in cells of the innate immune system—to instigate various inflammatory and adaptive immune pathways promoting, for example, acute and chronic allograft rejection.…”

Section: Ros‐mediated Postischemic Reperfusion Injurymentioning

confidence: 99%

Transplantation and Damage-Associated Molecular Patterns (DAMPs)

Land

Agostinis

Gasser

et al. 2016

American Journal of Transplantation

133

110

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Upon solid organ transplantation and during cancer immunotherapy, cellular stress responses result in the release of damage-associated molecular patterns (DAMPs). The various cellular stresses have been characterized in detail over the last decades, but a unifying classification based on clinically important aspects is lacking. Here, we provide an in-depth review of the most recent literature along with a unifying concept of the danger/injury model, suggest a classification of DAMPs, and review the recently elaborated mechanisms that result in the emission of such factors. We further point out the differences in DAMP responses including the release following a heat shock pattern, endoplasmic reticulum stress, DNA damage-mediated DAMP release, and discuss the diverse pathways of regulated necrosis in this respect. The understanding of various forms of DAMPs and the consequences of their different release patterns are prerequisite to associate serum markers of cellular stresses with clinical outcomes.

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Endoplasmic reticulum stress of Kupffer cells involved in the conversion of natural regulatory T cells to Th17 cells in liver ischemia‐reperfusion injury

Abstract: Endoplasmic reticulum stress of KCs contributed to the conversion of nTregs to Th17 cells due to interleukin-6, resulting in the worsening of liver insult.

Cited by 25 publications

References 26 publications

Distant organ dysfunction in acute kidney injury

Distant organ dysfunction in acute kidney injury

Origin and Consequences of Necroinflammation

Transplantation and Damage-Associated Molecular Patterns (DAMPs)

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