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High Mobility Group Box-1 (HMGB1) in a Neuroimmune Crosstalk
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High Mobility Group Box-1 (HMGB1) in a Neuroimmune Crosstalk

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 7423

Special Issue Editors

Prof. Dr. Atsufumi Kawabata

E-Mail Website
Guest Editor
Laboratory of Pharmacology and Pathophysiology/Faculty of Pharmacy, Kindai University, Higashi-Osaka 577-8502, Japan
Interests: high-mobility group box 1 (HMGB1); T-type calcium channel; hydrogen sulfide; proteinase-activated receptor (PAR); neuroinflammation; pain
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Masahiro Nishibori

E-Mail Website
Guest Editor
Department of Translational Research and Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan
Interests: HMGB1 Protein

Special Issue Information

Dear Colleagues,

High-mobility group box 1 (HMGB1), a nuclear protein, is passively released from dying cells, actively secreted by certain cells, and functions as a damage-associated molecular pattern protein. Extracellular HMGB1 directly or indirectly activates some pattern recognition receptors (PRRs), such as Toll-like receptors (TLR) 2 and 5, the receptor for advanced glycation end product (RAGE), CXC chemokine receptor 4 (CXCR4), etc., and plays multiple roles in health and disease. Given the release of HMGB1 from immune cells, including macrophages and also neurons that express HMGB1-targeted PRRs, HMGB1 is considered a mediator in the communication between immune cells and neurons. Such a neuroimmune crosstalk is essential for neuroinflammation, and is involved in the inception and/or progression of various CNS and PNS diseases, such as stroke, neurodegenerative and psychiatric disorders, and neuropathic pain. Therefore, this Special Issue focuses on the role of HMGB1 in neuroimmune interactions.

Prof. Dr. Atsufumi Kawabata
Prof. Dr. Masahiro Nishibori
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • damage-associated molecular patterns (DAMPs)
  • pattern recognition receptors (PRRs)
  • neuroinflammation
  • neurogenic inflammation

Published Papers (4 papers)

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Research

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13 pages, 2281 KiB  
Article
Repeated Social Defeat Stress Induces HMGB1 Nuclear Export in Prefrontal Neurons, Leading to Social Avoidance in Mice
by Shiho Kitaoka, Ayaka Tomohiro, Shinya Ukeshima, Keyue Liu, Hidenori Wake, Shinya H. Kimura, Yasuhiko Yamamoto, Masahiro Nishibori and Tomoyuki Furuyashiki
Cells 2023, 12(13), 1789; https://doi.org/10.3390/cells12131789 - 05 Jul 2023
Cited by 5 | Viewed by 1516
Abstract
Inflammation has been associated with depression, and innate immune receptors, such as the Toll-like receptor (TLR) 2/4 in the medial prefrontal cortex (mPFC), are crucial for chronic stress-induced depression-related behaviors in mice. HMGB1, a putative ligand for TLR2/4, has been suggested to promote [...] Read more.
Inflammation has been associated with depression, and innate immune receptors, such as the Toll-like receptor (TLR) 2/4 in the medial prefrontal cortex (mPFC), are crucial for chronic stress-induced depression-related behaviors in mice. HMGB1, a putative ligand for TLR2/4, has been suggested to promote depression-related behaviors under acute stress. However, the roles of endogenous HMGB1 under chronic stress remain to be investigated. Here, we found that the cerebroventricular infusion of HMGB1 proteins blocked stress-induced social avoidance and that HMGB1-neutralizing antibodies augmented repeated social defeat stress-induced social avoidance in mice, suggesting the antidepressive-like effect of HMGB1 in the brain. By contrast, the infusion of HMGB1-neutralizing antibodies to the mPFC and HMGB1 knockout in α-CaMKII-positive forebrain neurons attenuated the social avoidance, suggesting the pro-depressive-like effect of HMGB1 released from prefrontal neurons under chronic stress. In addition, repeated social defeat stress induced HMGB1 nuclear export selectively in mPFC neurons, which was abolished in the mice lacking RAGE, one of HMGB1 receptors, suggesting the positive feedback loop of HMGB1-RAGE signaling under chronic stress. These findings pave the way for identifying multiple roles of HMGB1 in the brain for chronic stress and depression. Full article
(This article belongs to the Special Issue High Mobility Group Box-1 (HMGB1) in a Neuroimmune Crosstalk)
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15 pages, 62803 KiB  
Article
Urothelial Oxidative Stress and ERK Activation Mediate HMGB1-Induced Bladder Pain
by Shaojing Ye, Dlovan F. D. Mahmood, Fei Ma, Lin Leng, Richard Bucala and Pedro L. Vera
Cells 2023, 12(10), 1440; https://doi.org/10.3390/cells12101440 - 22 May 2023
Cited by 1 | Viewed by 1196
Abstract
Activation of intravesical protease activated receptors-4 (PAR4) results in bladder pain through the release of urothelial macrophage migration inhibitory factor (MIF) and high mobility group box-1 (HMGB1). We aimed to identify HMGB1 downstream signaling events at the bladder that mediate HMGB1-induced bladder pain [...] Read more.
Activation of intravesical protease activated receptors-4 (PAR4) results in bladder pain through the release of urothelial macrophage migration inhibitory factor (MIF) and high mobility group box-1 (HMGB1). We aimed to identify HMGB1 downstream signaling events at the bladder that mediate HMGB1-induced bladder pain in MIF-deficient mice to exclude any MIF-related effects. We studied whether oxidative stress and ERK activation are involved by examining bladder tissue in mice treated with intravesical disulfide HMGB1 for 1 h and analyzed with Western blot and immunohistochemistry. HMGB1 intravesical treatment increased urothelium 4HNE and phospho-ERK1/2 staining, suggesting that HMGB1 increased urothelial oxidative stress and ERK activation. Furthermore, we examined the functional roles of these events. We evaluated lower abdominal mechanical thresholds (an index of bladder pain) before and 24 h after intravesical PAR4 or disulfide HMGB1. Intravesical pre-treatments (10 min prior) included: N-acetylcysteine amide (NACA, reactive oxygen species scavenger) and FR180204 (FR, selective ERK1/2 inhibitor). Awake micturition parameters (voided volume; frequency) were assessed at 24 h after treatment. Bladders were collected for histology at the end of the experiment. Pre-treatment with NACA or FR significantly prevented HMGB1-induced bladder pain. No significant effects were noted on micturition volume, frequency, inflammation, or edema. Thus, HMGB1 activates downstream urothelial oxidative stress production and ERK1/2 activation to mediate bladder pain. Further dissection of HMGB1 downstream signaling pathway may lead to novel potential therapeutic strategies to treat bladder pain. Full article
(This article belongs to the Special Issue High Mobility Group Box-1 (HMGB1) in a Neuroimmune Crosstalk)
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22 pages, 6168 KiB  
Article
Treatment of Marmoset Intracerebral Hemorrhage with Humanized Anti-HMGB1 mAb
by Dengli Wang, Daiki Ousaka, Handong Qiao, Ziyi Wang, Kun Zhao, Shangze Gao, Keyue Liu, Kiyoshi Teshigawara, Kenzo Takada and Masahiro Nishibori
Cells 2022, 11(19), 2970; https://doi.org/10.3390/cells11192970 - 23 Sep 2022
Cited by 2 | Viewed by 2074
Abstract
Intracerebral hemorrhage (ICH) is recognized as a severe clinical problem lacking effective treatment. High mobility group box-1 (HMGB1) exhibits inflammatory cytokine-like activity once released into the extracellular space from the nuclei. We previously demonstrated that intravenous injection of rat anti-HMGB1 monoclonal antibody (mAb) [...] Read more.
Intracerebral hemorrhage (ICH) is recognized as a severe clinical problem lacking effective treatment. High mobility group box-1 (HMGB1) exhibits inflammatory cytokine-like activity once released into the extracellular space from the nuclei. We previously demonstrated that intravenous injection of rat anti-HMGB1 monoclonal antibody (mAb) remarkably ameliorated brain injury in a rat ICH model. Therefore, we developed a humanized anti-HMGB1 mAb (OKY001) for clinical use. The present study examined whether and how the humanized anti-HMGB1 mAb ameliorates ICH injury in common marmosets. The results show that administration of humanized anti-HMGB1 mAb inhibited HMGB1 release from the brain into plasma, in association with a decrease of 4-hydroxynonenal (4-HNE) accumulation and a decrease in cerebral iron deposition. In addition, humanized anti-HMGB1 mAb treatment resulted in a reduction in brain injury volume at 12 d after ICH induction. Our in vitro experiment showed that recombinant HMGB1 inhibited hemoglobin uptake by macrophages through CD163 in the presence of haptoglobin, suggesting that the release of excess HMGB1 from the brain may induce a delay in hemoglobin scavenging, thereby allowing the toxic effects of hemoglobin, heme, and Fe2+ to persist. Finally, humanized anti-HMGB1 mAb reduced body weight loss and improved behavioral performance after ICH. Taken together, these results suggest that intravenous injection of humanized anti-HMGB1 mAb has potential as a novel therapeutic strategy for ICH. Full article
(This article belongs to the Special Issue High Mobility Group Box-1 (HMGB1) in a Neuroimmune Crosstalk)
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Review

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24 pages, 1503 KiB  
Review
High Mobility Group Box 1 (HMGB1): Potential Target in Sepsis-Associated Encephalopathy
by Bram DeWulf, Laurens Minsart, Franck Verdonk, Véronique Kruys, Michael Piagnerelli, Mervyn Maze and Sarah Saxena
Cells 2023, 12(7), 1088; https://doi.org/10.3390/cells12071088 - 04 Apr 2023
Cited by 3 | Viewed by 2060
Abstract
Sepsis-associated encephalopathy (SAE) remains a challenge for intensivists that is exacerbated by lack of an effective diagnostic tool and an unambiguous definition to properly identify SAE patients. Risk factors for SAE development include age, genetic factors as well as pre-existing neuropsychiatric conditions. Sepsis [...] Read more.
Sepsis-associated encephalopathy (SAE) remains a challenge for intensivists that is exacerbated by lack of an effective diagnostic tool and an unambiguous definition to properly identify SAE patients. Risk factors for SAE development include age, genetic factors as well as pre-existing neuropsychiatric conditions. Sepsis due to certain infection sites/origins might be more prone to encephalopathy development than other cases. Currently, ICU management of SAE is mainly based on non-pharmacological support. Pre-clinical studies have described the role of the alarmin high mobility group box 1 (HMGB1) in the complex pathogenesis of SAE. Although there are limited data available about the role of HMGB1 in neuroinflammation following sepsis, it has been implicated in other neurologic disorders, where its translocation from the nucleus to the extracellular space has been found to trigger neuroinflammatory reactions and disrupt the blood–brain barrier. Negating the inflammatory cascade, by targeting HMGB1, may be a strategy to complement non-pharmacologic interventions directed against encephalopathy. This review describes inflammatory cascades implicating HMGB1 and strategies for its use to mitigate sepsis-induced encephalopathy. Full article
(This article belongs to the Special Issue High Mobility Group Box-1 (HMGB1) in a Neuroimmune Crosstalk)
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