Role of TLR5 in inflammation and tissue damage after intestinal ischemia-reperfusion injury

Ito, Homare; Sadatomo, Ai; Inoue, Yoshiyuki; Yamada, Naoya; Aizawa, Emi; Hishida, Erika; Kamata, Ryo; Karasawa, Tadayoshi; Kimura, Hiroaki; Watanabe, Sachiko; Komada, Takanori; Horie, Hisanaga; Kitayama, Joji; Sata, Naohiro; Takahashi, Masafumi

doi:10.1016/j.bbrc.2019.08.083

Cited by 17 publications

(8 citation statements)

References 23 publications

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“…Inflammatory cascades and oxidative stress can then cause a cytokine storm, causing cell death caused by damage to cellular structures. I/R can trigger different mechanisms in tissue, leading to microvascular damage, cellular necrosis, or apoptosis [23,24].…”

Section: Discussionmentioning

confidence: 99%

“…While I/R that develops in mesenteric blood vessels often causes acute vascular insufficiency and local tissue damage, it can also cause multi-organ failure with high morbidity and mortality rates [4,5,24,25]. It has been shown that the lungs are particularly susceptible to distant organ damage due to intestinal I/R and I/R causes lung tissue damage [6].…”

Section: Discussionmentioning

confidence: 99%

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The Effects of Cannabinoid System on Acute Lung Injury Induced by Mesenteric Ischemia/Reperfusion in Rats

Yilmaz-Can¹

2021

IJOPRS

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Background: Cannabinoids are considered as key mediators in the pathophysiology of inflammatory diseases, including ischemia/reperfusion (I/R). However, there is no detailed information about the effects of cannabinoids on acute lung injury induced by mesenteric I/R in rats. The aim of this study is to investigate for the first time the possible effects of cannabinoid system on pathophysiological changes of acute lung injury induced by mesenteric I/R in rats. Materials and Methods:The superior mesenteric artery was blocked for 30min followed by 24h of reperfusion. Selective monoacylglycerol lipase inhibitor; JZL184, non selective cannabinoid receptor agonist; cannabidiol and selective CB2 agonist; JWH133 were administered to rats 30min before ischemia. At the end of the 24h reperfusion period, intestinal and lung tissues were removed; caspase 3, 8, 9 immunohistochemistry staining, caspase-3 activity and malondialdehyde (MDA) levels were evaluated. Serum IL-1, TNF-α, IL-6 levels and total antioxidant capacity (TAC) also measured. Results:In intestine tissue; decrease in intestinal mucosal damage was detected with all three therapeutic agents but it was not statistically significant. Cannabidiol and JZL184 significantly reduced caspase 3, 8 and 9 immunohistochemical staining. In lung tissue; Cannabidiol significantly reduced caspase 3, 8 and 9 immunohistochemical staining while JZL184 significantly reduced caspase 8 staining. JZL184 significantly reduced alveolar congestion, haemorrhage, neutrophilic infiltration and alveolar wall thickening while JWH133 significantly reduced neutrophilic infiltration and alveolar wall thickness. No significant differences were observed in terms of biochemical parameters in the control and ischemiareperfusion groups. Conclusion:This study has shown that the cannabinoid system may be a therapeutic target for attenuation and/or treatment of inflammatory lung diseases induced by mesenteric I/R

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The Effects of Cannabinoid System on Acute Lung Injury Induced by Mesenteric Ischemia/Reperfusion in Rats

Yilmaz-Can¹

2021

IJOPRS

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“…Therefore, the HMGB1/TLR4/NF-κB pathway is an important pathway to induce inflammatory response and oxidative stress. In addition, TLR5 has been reported to be highly expressed in inflammatory diseases and tissues, and TLR5 knockdown significantly decreased the release of inflammatory cytokines (Gao et al 2019 ; Ito et al 2019 ). Moreover, TLR5 could activate NF-κB pathway (Yan et al 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Lycorine attenuates lipopolysaccharide-induced acute lung injury through the HMGB1/TLRs/NF-κB pathway

Meng

Fei

et al. 2020

3 Biotech

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Lung injury associated with systemic inflammatory response is a common problem affecting human health. Previous studies have shown that lycorine exerts a anti-inflammatory effect. However, whether lycorine alleviates lung injury remains unclear. To explore this issue, BALB/c mice and MLE-12 cells were treated with lipopolysaccharide (LPS) to establish lung injury mouse model and cell model, respectively. Glycyrrhizic acid, known as an inhibitor of ALI, was also used to study the effects of lycorine in vitro. Our results showed that after LPS treatment, the lung injury score, lung wet-to-dry weight ratio, and malondialdehyde (MDA) production in the lung tissues and the expression levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6 in bronchoalveolar lavage fluid were significantly increased, whereas their levels were decreased by lycorine. Additionally, LPS injection activated the high-mobility group box 1 (HMGB1)/Toll-like receptors (TLRs)/NF-κB pathway. However, lycorine treatment attenuated the activity of the HMGB1/TLRs/NF-κB pathway in the lung tissues. In vitro studies showed that lycorine administration significantly decreased the levels of inflammatory cytokines and MDA and attenuated the activity of the HMGB1/TLRs/NF-κB pathway in LPS-treated cells. Moreover, the inhibitory effects of lycorine on the inflammatory response and oxidative stress in LPS-treated lung cells were similar with that of glycyrrhizic acid, and this inhibition was intensified by both lycorine and glycyrrhizic acid treatment. We suggest that lycorine could alleviate LPS-induced lung injury of inflammation and oxidative stress by blocking the HMGB1/TLRs/NF-κB pathway, which gives a new perspective for ALI therapy to treat lycorine as a potential treatment clinically.

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“…Intestinal IRI is a common life-threatening complication that can present with the advent of mesenteric artery thrombosis, strangulated intestinal obstruction, trauma, abdominal aortic aneurysm surgery and bowel transplantation. 29 Therefore, it is imperative to improve the current means of alleviating intestinal IRI. Existing evidence suggests that dexmedetomidine confers a protective effect on IRI in coronary artery endothelial dysfunction in heart.…”

Section: Dexmedetomidine Treatment Protected Rats Against Intestinal Irimentioning

confidence: 99%

Dexmedetomidine reduces enteric glial cell injury induced by intestinal ischaemia‐reperfusion injury through mitochondrial localization of TERT

Liu

et al. 2022

J Cellular Molecular Medi

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This study was performed to uncover the effects of dexmedetomidine on oxidative stress injury induced by mitochondrial localization of telomerase reverse transcriptase (TERT) in enteric glial cells (EGCs) following intestinal ischaemia‐reperfusion injury (IRI) in rat models. Following establishment of intestinal IRI models by superior mesenteric artery occlusion in Wistar rats, the expression and distribution patterns of TERT were detected. The IRI rats were subsequently treated with low or high doses of dexmedetomidine, followed by detection of ROS, MDA and GSH levels. Calcein cobalt and rhodamine 123 staining were also carried out to detect mitochondrial permeability transition pore (MPTP) and the mitochondrial membrane potential (MMP), respectively. Moreover, oxidative injury of mtDNA was determined, in addition to analyses of EGC viability and apoptosis. Intestinal tissues and mitochondria of EGCs were badly damaged in the intestinal IRI group. In addition, there was a reduction in mitochondrial localization of TERT, oxidative stress, whilst apoptosis of EGCs was increased and proliferation was decreased. On the other hand, administration of dexmedetomidine was associated with promotion of mitochondrial localization of TERT, whilst oxidative stress, MPTP and mtDNA in EGCs, and EGC apoptosis were all inhibited, and the MMP and EGC viability were both increased. A positive correlation was observed between different doses of dexmedetomidine and protective effects. Collectively, our findings highlighted the antioxidative effects of dexmedetomidine on EGCs following intestinal IRI, as dexmedetomidine alleviated mitochondrial damage by enhancing the mitochondrial localization of TERT.

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Role of TLR5 in inflammation and tissue damage after intestinal ischemia-reperfusion injury

Cited by 17 publications

References 23 publications

The Effects of Cannabinoid System on Acute Lung Injury Induced by Mesenteric Ischemia/Reperfusion in Rats

The Effects of Cannabinoid System on Acute Lung Injury Induced by Mesenteric Ischemia/Reperfusion in Rats

Lycorine attenuates lipopolysaccharide-induced acute lung injury through the HMGB1/TLRs/NF-κB pathway

Dexmedetomidine reduces enteric glial cell injury induced by intestinal ischaemia‐reperfusion injury through mitochondrial localization of TERT

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