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Chronic Diseases: Gut-Brain-Immune-Microbiome Axis
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Chronic Diseases: Gut-Brain-Immune-Microbiome Axis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 21287

Special Issue Editor

Prof. Dr. Vasso Apostolopoulos

E-Mail Website
Guest Editor
Institute for Health and Sport, Victoria University, Melbourne, VIC 3011, Australia
Interests: immunology; protein crystallography; medicinal chemistry; cellular and molecular biology; extensive translational research; clinical trials; vaccines; drugs; healthy ageing; chronic diseases; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

The associations between gut microbiome composition and disease status have been widely reported, while recent studies have demonstrated a role for the gut microbiome in influencing remote organs, mucosal, and immune function.

Permeability or leakiness of the intestinal epithelial barrier contributes to the development and/or severity of multiple chronic diseases, including but not limited to obesity, diabetes, certain types of cancer, liver dysfunction, neurological conditions (via the gut–brain axis), stroke, etc. Furthermore, gastrointestinal function, including epithelial cell integrity and turnover, regulation of mucus production, anti-microbial and mucosal immune defense, microbiome function, and microbe–host communication, not only contribute to epithelial barrier dysfunction but are also susceptible to dietary interventions.

Disease immunity is inseparable from the feedback and regulation of the nervous system. Chronic diseases caused by the nervous system itself, including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis and epilepsy, and even substance abuse, use also afflict people.

This Special Issue focuses on chronic diseases, not only neurochronic diseases, but also diabetes, heart disease, arthritis, gastrointestinal diseases, inflammatory diseases, autoimmune diseases, etc. The absorption and barrier functions of the stomach and intestines play a role in immune and neuromodulatory aspects of disease immunity. We welcome your original research or review papers on cellular and molecular aspects of the gut–brain–immune–microbiome axis as well as chronic conditions.

Prof. Dr. Vasso Apostolopoulos
Guest Editor

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Keywords

  • epithelial barrier integrity
  • mucosal immune function
  • immune tolerance
  • intestinal flora
  • celiac disease
  • intestinal barrier
  • neurochronic diseases
  • diabetes
  • heart disease
  • arthritis
  • gastroenteritis
  • inflammatory bowel disease
  • addiction
  • headache
  • inflammation
  • chronic diseases

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Published Papers (3 papers)

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Research

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18 pages, 9424 KiB  
Article
Lipocalin-2 Deficiency Diminishes Canonical NLRP3 Inflammasome Formation and IL-1β Production in the Subacute Phase of Spinal Cord Injury
by Nina Müller, Miriam Scheld, Clara Voelz, Natalie Gasterich, Weiyi Zhao, Victoria Behrens, Ralf Weiskirchen, Maryam Baazm, Tim Clarner, Cordian Beyer, Nima Sanadgol and Adib Zendedel
Int. J. Mol. Sci. 2023, 24(10), 8689; https://doi.org/10.3390/ijms24108689 - 12 May 2023
Cited by 10 | Viewed by 2229
Abstract
Spinal cord injury (SCI) results in the production of proinflammatory cytokines due to inflammasome activation. Lipocalin 2 (LCN2) is a small secretory glycoprotein upregulated by toll-like receptor (TLR) signaling in various cells and tissues. LCN2 secretion is induced by infection, injury, and metabolic [...] Read more.
Spinal cord injury (SCI) results in the production of proinflammatory cytokines due to inflammasome activation. Lipocalin 2 (LCN2) is a small secretory glycoprotein upregulated by toll-like receptor (TLR) signaling in various cells and tissues. LCN2 secretion is induced by infection, injury, and metabolic disorders. In contrast, LCN2 has been implicated as an anti-inflammatory regulator. However, the role of LCN2 in inflammasome activation during SCI remains unknown. This study examined the role of Lcn2 deficiency in the NLRP3 inflammasome-dependent neuroinflammation in SCI. Lcn2−/− and wild-type (WT) mice were subjected to SCI, and locomotor function, formation of the inflammasome complex, and neuroinflammation were assessed. Our findings demonstrated that significant activation of the HMGB1/PYCARD/caspase-1 inflammatory axis was accompanied by the overexpression of LCN2 7 days after SCI in WT mice. This signal transduction results in the cleaving of the pyroptosis-inducing protein gasdermin D (GSDMD) and the maturation of the proinflammatory cytokine IL-1β. Furthermore, Lcn2−/− mice showed considerable downregulation in the HMGB1/NLRP3/PYCARD/caspase-1 axis, IL-1β production, pore formation, and improved locomotor function compared with WT. Our data suggest that LCN2 may play a role as a putative molecule for the induction of inflammasome-related neuroinflammation in SCI. Full article
(This article belongs to the Special Issue Chronic Diseases: Gut-Brain-Immune-Microbiome Axis)
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24 pages, 5799 KiB  
Article
Methamphetamine Induces Systemic Inflammation and Anxiety: The Role of the Gut–Immune–Brain Axis
by Majid Davidson, Marina Mayer, Amanda Habib, Niloufar Rashidi, Rhiannon Talia Filippone, Sarah Fraser, Monica D. Prakash, Puspha Sinnayah, Kathy Tangalakis, Michael L. Mathai, Kulmira Nurgali and Vasso Apostolopoulos
Int. J. Mol. Sci. 2022, 23(19), 11224; https://doi.org/10.3390/ijms231911224 - 23 Sep 2022
Cited by 20 | Viewed by 11041
Abstract
Methamphetamine (METH) is a highly addictive drug abused by millions of users worldwide, thus becoming a global health concern with limited management options. The inefficiency of existing treatment methods has driven research into understanding the mechanisms underlying METH-induced disorders and finding effective treatments. [...] Read more.
Methamphetamine (METH) is a highly addictive drug abused by millions of users worldwide, thus becoming a global health concern with limited management options. The inefficiency of existing treatment methods has driven research into understanding the mechanisms underlying METH-induced disorders and finding effective treatments. This study aims to understand the complex interactions of the gastrointestinal–immune–nervous systems following an acute METH dose administration as one of the potential underlying molecular mechanisms concentrating on the impact of METH abuse on gut permeability. Findings showed a decreased expression of tight junction proteins ZO-1 and EpCAm in intestinal tissue and the presence of FABP-1 in sera of METH treated mice suggests intestinal wall disruption. The increased presence of CD45+ immune cells in the intestinal wall further confirms gut wall inflammation/disruption. In the brain, the expression of inflammatory markers Ccl2, Cxcl1, IL-1β, TMEM119, and the presence of albumin were higher in METH mice compared to shams, suggesting METH-induced blood–brain barrier disruption. In the spleen, cellular and gene changes are also noted. In addition, mice treated with an acute dose of METH showed anxious behavior in dark and light, open field, and elevated maze tests compared to sham controls. The findings on METH-induced inflammation and anxiety may provide opportunities to develop effective treatments for METH addiction in the future. Full article
(This article belongs to the Special Issue Chronic Diseases: Gut-Brain-Immune-Microbiome Axis)
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Review

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25 pages, 2153 KiB  
Review
Circadian Disruption and Mental Health: The Chronotherapeutic Potential of Microbiome-Based and Dietary Strategies
by Pilar Codoñer-Franch, Marie Gombert, José Martínez-Raga and María Carmen Cenit
Int. J. Mol. Sci. 2023, 24(8), 7579; https://doi.org/10.3390/ijms24087579 - 20 Apr 2023
Cited by 10 | Viewed by 7168
Abstract
Mental illness is alarmingly on the rise, and circadian disruptions linked to a modern lifestyle may largely explain this trend. Impaired circadian rhythms are associated with mental disorders. The evening chronotype, which is linked to circadian misalignment, is a risk factor for severe [...] Read more.
Mental illness is alarmingly on the rise, and circadian disruptions linked to a modern lifestyle may largely explain this trend. Impaired circadian rhythms are associated with mental disorders. The evening chronotype, which is linked to circadian misalignment, is a risk factor for severe psychiatric symptoms and psychiatric metabolic comorbidities. Resynchronization of circadian rhythms commonly improves psychiatric symptoms. Furthermore, evidence indicates that preventing circadian misalignment may help reduce the risk of psychiatric disorders and the impact of neuro–immuno–metabolic disturbances in psychiatry. The gut microbiota exhibits diurnal rhythmicity, as largely governed by meal timing, which regulates the host’s circadian rhythms. Temporal circadian regulation of feeding has emerged as a promising chronotherapeutic strategy to prevent and/or help with the treatment of mental illnesses, largely through the modulation of gut microbiota. Here, we provide an overview of the link between circadian disruption and mental illness. We summarize the connection between gut microbiota and circadian rhythms, supporting the idea that gut microbiota modulation may aid in preventing circadian misalignment and in the resynchronization of disrupted circadian rhythms. We describe diurnal microbiome rhythmicity and its related factors, highlighting the role of meal timing. Lastly, we emphasize the necessity and rationale for further research to develop effective and safe microbiome and dietary strategies based on chrononutrition to combat mental illness. Full article
(This article belongs to the Special Issue Chronic Diseases: Gut-Brain-Immune-Microbiome Axis)
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