Ali Mehdizadeh1, Vahid Shaygannejad2*, Meysam Amidfar3, Seyed Javad Hasheminia4, Mohamad Mousaei Ghasroldasht5
1School of medicine, Isfahan University of medical sciences, Isfahan, Iran.
2Isfahan neuroscience research center, alzahra research institute, Isfahan University of medical sciences, Isfahan, Iran.
3Tehran University of medical sciences, Tehran, Iran
4Department of immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
5Biology department, shahid ashrafi Isfahan University, clinical laboratory, alzahra hospital, Isfahan, Iran.
Background: interleukin-23 (IL-23) is a member of the IL-12 cytokine family that has shown through enhancement of T helper type 17 (Th17) cells expansion could play an important role in the inflammatory autoimmune responses in multiple sclerosis (MS).
Methods: The objective of the present study is to measure the relative expression of IL-23 mRNA in the peripheral blood of 15 MS patients in comparison with 15 healthy control subjects.
Results: the relative gene expression level of IL-23 in the peripheral blood cells from MS Patients was significantly increased compared to healthy controls (p < 0.001).
Conclusions: Our findings revealed upregulated gene expression pattern of IL-23 in the peripheral blood of MS patients that may be a peripheral marker for diagnosis of MS and might be a novel and promising therapeutic target for MS.DOI: 10.29245/2578-3009/2018/4.1147 View / Download Pdf View Full Text
Nasim Rahmani Kukia1, Payam Zandi2, Ardeshir Abbasi3*
1Department of Microbiology, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran
2Department of Medical Biotechnology, Faculty of Medical Sciences, Tarbiat Modares University Tehran, Iran
3Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
Mesenchymal stromal cells(MSCs) have been exploited for their immunomodulatory properties in treating various immune-related disorders. MSCs can modulate the immune system through interactions with a variety of immune cells. Regardless of the researchers focused on understanding how MSCs connect to individual immune system cell subsets, the mechanisms for inducing restorative effect still stay mainly undiscovered. Through this mini-review we address what is known about the associations and effects of educated MSCs with cells of the innate immune system (macrophages and neutrophils) and our knowledge of these interactions will be essential in increasing and expanding new medical protocols for MSC based cell therapy in the foreseeable future.DOI: 10.29245/2578-3009/2018/4.1149 View / Download Pdf View Full Text
Atsushi Anzai*, Motoaki Sano
Department of Cardiology, Keio University School of Medicine, Tokyo, Japan
In-hospital outcomes are generally acceptable with the conservative treatment of uncomplicated type B aortic dissection, but some patients present with undesirable complications, such as aortic expansion and rupture. Beyond mechanical and shear forces of blood flow affecting the weakened aortic wall, excessive inflammatory response has been shown to be associated with aortic expansion and adverse clinical outcomes. We have previously demonstrated the underlying mechanisms of catastrophic complications after acute aortic dissection (AAD) in mice. We propose that aortic dissection induces expression of the neutrophil chemoattractants CXCL1 and granulocyte-colony stimulating factor in the aortic tunica adventitia. These local environmental changes recruit neutrophils in combination with alteration of bone marrow milieu where reduced CXCL12 expression enhances neutrophil egress. Interleukin (IL)-6 production in the inflammatory adventitial neutrophils causes vascular inflammation, leading to vascular wall fragility. Targeting CXCR2 or IL-6 mitigates aortic expansion and prevents mice from aortic rupture. Collectively, adventitial neutrophil-mediated inflammation may be a potential therapeutic target to limit lethal complications after AAD.DOI: 10.29245/2578-3009/2018/4.1156 View / Download Pdf View Full Text
Hillary W. Bedell1,2 and Jeffrey R. Capadona1,2*
1Department of Biomedical Engineering, Case Western Reserve University, School of Engineering, 2071 MLK Jr. Drive, Wickenden Bldg, Cleveland OH 44106, USA
2Advanced Platform Technology Center, L. Stokes Cleveland VA Medical Center, Rehab. R&D, 10701 East Blvd. Mail Stop 151 AW/APT, Cleveland OH 44106, USA
Intracortical microelectrodes are used both in basic research to increase our understanding of the nervous system and for rehabilitation purposes through brain-computer interfaces. Yet, challenges exist preventing the widespread clinical use of this technology. A prime challenge is with the neuroinflammatory response to intracortical microelectrodes. This mini-review details immunomodulatory strategies employed to decrease the inflammatory response to these devices. Over time, broad-spectrum anti-inflammatory approaches, such as dexamethasone and minocycline, evolved into more targeted treatments since the underlying biology of the neuroinflammation was elucidated. This review also presents studies which examine novel prospective targets for future immunomodulatory targeting.DOI: 10.29245/2578-3009/2018/4.1157 View / Download Pdf View Full Text