Probiotics ameliorate renal ischemia-reperfusion injury by modulating the phenotype of macrophages through the IL-10/GSK-3β/PTEN signaling pathway

Ding, Chenguang; Han, Feng; Xiang, Hao; Wang, Yuxiang; Li, Yang; Zheng, Jin; Xue, Wujun; Ding, Xiaoming; Tian, Puxun

doi:10.1007/s00424-018-2213-1

Cited by 28 publications

(21 citation statements)

References 20 publications

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“…Several studies have followed this in different populations confirming that these alterations are fairly consistent across cultural and ethnic borders [204,205,286,305] [222,223,289] the models have been generally quite potent and proximal to the intestine including using MUC2 deficient mice and DSS [222,308]. Interestingly, a similar study to our own was conducted using male Wistar rats and administered VSL#3 daily for two weeks prior to the induction of renal ischemia reperfusion injury [290]. This study did not examine changes in the microbiota; however, the researchers analysed several of the same factors including IL-1B, IL-6 and found generally lowered levels of myeloid cell activation, reduced pro-inflammatory signalling and reduced tissue damage following renal ischemic re-perfusion [290].…”

Section: Dss Treatment Increased Intestinal Tnf-α and Il-1β Mrna Exprsupporting

confidence: 54%

“…Interestingly, a similar study to our own was conducted using male Wistar rats and administered VSL#3 daily for two weeks prior to the induction of renal ischemia reperfusion injury [290]. This study did not examine changes in the microbiota; however, the researchers analysed several of the same factors including IL-1B, IL-6 and found generally lowered levels of myeloid cell activation, reduced pro-inflammatory signalling and reduced tissue damage following renal ischemic re-perfusion [290]. These findings stand in stark contrast with our own, perhaps suggesting a difference in the physiology of C57BL/6 mice compared to Wistar rats, or more likely, could be related to the different toxins used in the present study.…”

Section: Dss Treatment Increased Intestinal Tnf-α and Il-1β Mrna Exprmentioning

confidence: 73%

“…is a probiotic which is currently prescribed for irritable bowel syndrome and has been shown to reduce stressor-linked effects in animal models and can modulate intestinal permeability [222,225]. Two recent papers have also found that VSL#3 may play a protective role in visceral hypersensitivity [289] and renal ischemia injuries [290] by modulating immune cell phenotypes.…”

Section: Introductionmentioning

confidence: 99%

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Environmental toxicant exposure and Parkinson’s disease: LRRK2 and inflammatory processes

Dwyer¹

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Parkinson's disease (PD) results from the progressive loss of dopamine producing neurons in the Substantia Nigra pars comapcta (SNc). This loss is thought to occur over several years to decades and current evidence suggests that neuroinflammation may play a central role in this loss. Numerous epidemiological studies have implicated chronic exposure to environmental toxicants such as heavy metals and pesticides to risk of developing PD. Indeed, many of these risk factors have been validated as rodent models of PD, able to induce dopaminergic cell loss in the SNc as well as motor dysfunction. While research strongly supports a role for environmental toxicants and inflammation in PD relatively little work has examined the interactions between these toxicants and other risk factors including senescence, genetic vulnerabilities, the gut microbiota or iii This thesis is based upon the following four manuscripts referred to in text by their corresponding chapter numbers.

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Section: Dss Treatment Increased Intestinal Tnf-α and Il-1β Mrna Exprsupporting

confidence: 54%

Section: Dss Treatment Increased Intestinal Tnf-α and Il-1β Mrna Exprmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 99%

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Environmental toxicant exposure and Parkinson’s disease: LRRK2 and inflammatory processes

Dwyer¹

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“…However, it failed to prevent AKI after cardiovascular surgery in patients [ 46 ]. Probiotics ameliorate I/R-induced AKI by increasing M2 macrophages in rats [ 47 ]. However, it has been demonstrated that the density of CD163 + M2 macrophages in the human kidney correlates with the severity of a variety of renal diseases, including: AKI [ 48 ], acute tubular injury [ 49 ], IgA nephropathy [ 50 ], chronic kidney allograft injury [ 51 ], and lupus nephritis [ 52 ].…”

Section: The Differences In Innate Immunity Among Rodents Large Animmentioning

confidence: 99%

Large animal models for translational research in acute kidney injury

et al. 2020

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While extensive research using animal models has improved the understanding of acute kidney injury (AKI), this knowledge has not been translated into effective treatments. Many promising interventions for AKI identified in mice and rats have not been validated in subsequent clinical trials. As a result, the mortality rate of AKI patients remains high. Inflammation plays a fundamental role in the pathogenesis of AKI, and one reason for the failure to translate promising therapeutics may lie in the profound difference between the immune systems of rodents and humans. The immune systems of large animals such as swine, nonhuman primates, sheep, dogs and cats, more closely resemble the human immune system. Therefore, in the absence of a basic understanding of the pathophysiology of human AKI, large animals are attractive models to test novel interventions. However, there is a lack of reviews on large animal models for AKI in the literature. In this review, we will first highlight differences in innate and adaptive immunities among rodents, large animals, and humans in relation to AKI. After illustrating the potential merits of large animals in testing therapies for AKI, we will summarize the current state of the evidence in terms of what therapeutics have been tested in large animal models. The aim of this review is not to suggest that murine models are not valid to study AKI. Instead, our objective is to demonstrate that large animal models can serve as valuable and complementary tools in translating potential therapeutics into clinical practice.

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“…Thermophilus) which is currently prescribed for irritable bowel syndrome and has been shown to modulate intestinal permeability [28,29]. Recent papers have also found that VSL#3 may play a protective role in visceral hypersensitivity [30] and renal ischemia injuries [31] by modulating immune cell phenotypes. In contrast, agents that irritate the gut and cause inflammation are thought to negatively affect the microbiome and could possibly contribute to PD.…”

Section: Introductionmentioning

confidence: 99%

The impact of dextran sodium sulphate and probiotic pre-treatment in a murine model of Parkinson’s disease

Dwyer

Chaiquin

Ayoub

et al. 2021

J Neuroinflammation

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Background Recent work has established that Parkinson’s disease (PD) patients have an altered gut microbiome, along with signs of intestinal inflammation. This could help explain the high degree of gastric disturbances in PD patients, as well as potentially be linked to the migration of peripheral inflammatory factors into the brain. To our knowledge, this is the first study to examine microbiome alteration prior to the induction of a PD murine model. Methods We presently assessed whether pre-treatment with the probiotic, VSL #3, or the inflammatory inducer, dextran sodium sulphate (DSS), would influence the PD-like pathology provoked by a dual hit toxin model using lipopolysaccharide (LPS) and paraquat exposure. Results While VSL #3 has been reported to have anti-inflammatory effects, DSS is often used as a model of colitis because of the gut inflammation and the breach of the intestinal barrier that it induces. We found that VSL#3 did not have any significant effects (beyond a blunting of LPS paraquat-induced weight loss). However, the DSS treatment caused marked changes in the gut microbiome and was also associated with augmented behavioral and inflammatory outcomes. In fact, DSS markedly increased taxa belonging to the Bacteroidaceae and Porphyromonadaceae families but reduced those from Rikencellaceae and S24-7, as well as provoking colonic pro-inflammatory cytokine expression, consistent with an inflamed gut. The DSS also increased the impact of LPS plus paraquat upon microglial morphology, along with circulating lipocalin-2 (neutrophil marker) and IL-6. Yet, neither DSS nor VSL#3 influenced the loss of substantia nigra dopamine neurons or the astrocytic and cytoskeleton remodeling protein changes that were provoked by the LPS followed by paraquat treatment. Conclusions These data suggest that disruption of the intestinal integrity and the associated microbiome can interact with systemic inflammatory events to promote widespread brain-gut changes that could be relevant for PD and at the very least, suggestive of novel neuro-immune communication.

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Probiotics ameliorate renal ischemia-reperfusion injury by modulating the phenotype of macrophages through the IL-10/GSK-3β/PTEN signaling pathway

Cited by 28 publications

References 20 publications

Environmental toxicant exposure and Parkinson’s disease: LRRK2 and inflammatory processes

Environmental toxicant exposure and Parkinson’s disease: LRRK2 and inflammatory processes

Large animal models for translational research in acute kidney injury

The impact of dextran sodium sulphate and probiotic pre-treatment in a murine model of Parkinson’s disease

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