Association between HMGB1 and COPD: A Systematic Review

Gangemi, Sebastiano; Casciaro, Marco; Trapani, Giovanni Di; Quartuccio, S.; Navarra, Michele; Pioggia, Giovanni; Imbalzano, Egidio

doi:10.1155/2015/164913

Cited by 44 publications

(38 citation statements)

References 45 publications

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“…In the present study, the HMGB1 expression in the lung tissues of the COPD model rats was significantly higher than in the control group, indicating that HMGB1 may participate in promoting the onset of COPD. The data are consistent with the studies conducted by Kanazawa et al (30) and Gangemi et al (15). Furthermore, the study by Li et al (31) determined that, compared with in the healthy control population, TRL4 expression in the bronchoalveolar lavage fluid of patients with COPD was significantly high.…”

Section: Discussionsupporting

confidence: 90%

“…In 1999, Wang et al (12) revealed for the first time, to the best of our knowledge, that HMGB1 is involved in sepsis, and can be considered an important inflammatory mediator. A number of previous studies revealed that ulinastatin could inhibit the release of the inflammatory mediator HMGB1 (8,13,14), and, therefore, it could be associated with COPD due to the high expression of HMGB1 in COPD (15). Toll-like receptor 4 (TLR4) is the receptor for HMGB1; the pro-inflammatory role of HMGB1 is closely associated with the TLR4 signal transduction pathway (16,17).…”

Section: Introductionmentioning

confidence: 99%

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Ulinastatin protects the lungs of COPD rats through the HMGB1/TLR4 signaling pathway

Liu

Zhang

et al. 2018

Oncol Lett

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The present study aimed to investigate the protective mechanism of ulinastatin against lung injury. Rat models with chronic obstructive pulmonary disease (COPD) were used to provide guidance for the medical treatment of this disease. The rats were divided into three groups: A control group, a model group and an experimental group (each, n=10). With the exception of the control group, all of the rats were prepared as models of COPD, using the composite molding method of smoking and intratracheal instillation of lipopolysaccharide. The rats in the model group all received a conventional treatment, while the rats in the experimental group received ulinastatin. A small animal lung function detector was used to examine lung function. The forced expiratory volume/sec (FEV) was negatively correlated with the protein expression levels of Toll-like receptor 4 (TLR4) and high mobility group box protein 1 (HMGB1). Real-time fluorescence quantitative polymerase chain reaction and western blot analyses were used to detect TLR4, MyD88 (myeloid differentiation factor 88), TRAF-6 (TNF receptor-associated factor 6), LOX-1 (lectin-type oxidized LDL receptor 1) and HMGB1 mRNA, along with their protein expression levels. The lung function of rats in the model group was significantly decreased compared with in the control group (P<0.05). In the experimental group the lung function was significantly greater, when compared with in the model group; however, it remained lower than in the control group. The mRNA and protein expression levels of TLR4, MyD88, TRAF-6, LOX-1 and HMGB1 were significantly higher in the model group than in the control and experimental groups; however, levels in the experimental group were significantly higher when compared with in the control group (P<0.05). The TLR4 and HMGB1 expression levels were positively correlated in all groups, which indicated involvement of the HMGB1/TLR4 signaling pathway. The FEV was negatively correlated with the protein expression levels of TLR4 and HMGB1. Thus, the protective effect of ulinastatin in the lungs of rats with COPD is associated with changes in the HMGB1/TLR4 signaling pathway.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Ulinastatin protects the lungs of COPD rats through the HMGB1/TLR4 signaling pathway

Liu

Zhang

et al. 2018

Oncol Lett

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“…In a previous literature review we demonstrated how HMGB-1 levels were augmented in different tissues of smokers and COPD patients [8]. Severe asthma subjects had higher sputum levels of HMGB-1 than moderate and mild patients.…”

Section: Discussionmentioning

confidence: 96%

Association between HMGB1 and asthma: a literature review

et al. 2017

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BackgroundRecently, some studies demonstrated that HMGB1, as proinflammatory mediator belonging to the alarmin family, has a key role in different acute and chronic immune disorders. Asthma is a complex disease characterised by recurrent and reversible airflow obstruction associated to airway hyper-responsiveness and airway inflammation.ObjectiveThis literature review aims to analyse advances on HMGB1 role, employment and potential diagnostic application in asthma.MethodsWe reviewed experimental studies that investigated the pathogenetic role of HMGB in bronchial airway hyper-responsiveness, inflammation and the correlation between HMGB1 level and asthma.ResultsA total of 19 studies assessing the association between HMGB1 and asthma were identified.ConclusionsWhat emerged from this literature review was the confirmation of HMGB-1 involvement in diseases characterised by chronic inflammation, especially in pulmonary pathologies. Findings reported suggest a potential role of the alarmin in being a stadiation method and a marker of therapeutic efficacy; finally, inhibiting HMGB1 in humans in order to contrast inflammation should be the aim for future further studies.

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“…Extracellular HMGB1 binds to cell surface receptors, such as RAGE, which activates the NF-kB pathway. As a consequence, activation of the HMGB1/RAGE/NF-kB pathway increases the expression of a wide variety of inflammatory mediators, escalates the acute inflammatory response, and increases apoptosis in vivo (Gangemi et al, 2015). It is also known that the HMGB1/RA-GE/NF-kB pathway could be regulated by oxidative stress Fig.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Myeloperoxidase by N-Acetyl Lysyltyrosylcysteine Amide Reduces Oxidative Stress–Mediated Inflammation, Neuronal Damage, and Neural Stem Cell Injury in a Murine Model of Stroke

Liang

Zheng

et al. 2017

J Pharmacol Exp Ther

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Recent studies suggest that myeloperoxidase (MPO)-dependent oxidative stress plays a significant role in brain injury in stroke patients. We previously showed that -acetyl lysyltyrosylcysteine amide (KYC), a novel MPO inhibitor, significantly decreased infarct size, blood-brain barrier leakage, infiltration of myeloid cells, loss of neurons, and apoptosis in the brains of middle cerebral artery occlusion (MCAO) mice. Inhibition of MPO also noticeably reduced neurologic severity scores of MCAO mice. Thus, our data support the idea that MPO-dependent oxidative stress plays a detrimental role in tissue injury in ischemic stroke. However, the mechanisms of MPO-induced injury in stroke are still largely unknown. Here, we present new evidence showing that KYC treatment greatly reduced inflammation by decreasing the number of proinflammatory M1 microglial cells and N1 neutrophils in the brains of MCAO mice. KYC also markedly reduced the expression of high-mobility group box 1, receptor for advanced glycation end products, and nuclear factor-B in the brains of MCAO mice. Both neurons and neural stem cells (NSCs) were oxidatively injured by MPO-dependent oxidative stress in MCAO mice. Inhibiting MPO-dependent oxidative stress with KYC significantly reduced oxidative injury and apoptosis in neurons and NSCs. KYC treatment also protected transplanted exogenous NSCs in the brains of MCAO mice. Thus, our studies suggest that MPO-dependent oxidative stress directly injures brain tissues by oxidizing neurons and NSCs and increasing inflammation during stroke. Inhibition of MPO activity with KYC preserves neuronal function and helps the brain recover from injury after stroke.

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Association between HMGB1 and COPD: A Systematic Review

Cited by 44 publications

References 45 publications

Ulinastatin protects the lungs of COPD rats through the HMGB1/TLR4 signaling pathway

Ulinastatin protects the lungs of COPD rats through the HMGB1/TLR4 signaling pathway

Association between HMGB1 and asthma: a literature review

Inhibition of Myeloperoxidase by N-Acetyl Lysyltyrosylcysteine Amide Reduces Oxidative Stress–Mediated Inflammation, Neuronal Damage, and Neural Stem Cell Injury in a Murine Model of Stroke

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