Ti–O based nanomaterials ameliorate experimental autoimmune encephalomyelitis and collagen-induced arthritis

RSC Advances ◽  
2016 ◽  
Vol 6 (11) ◽  
pp. 8870-8880 ◽  
Author(s):  
T. Sree Latha ◽  
Dakshayani Lomada ◽  
Praveen Kumar Dharani ◽  
Shankar V. Muthukonda ◽  
Madhava C. Reddy
Keyword(s):  
Rheumatoid Arthritis ◽  
Multiple Sclerosis ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Therapeutic Approach ◽  
Clinical Severity ◽  
Collagen Induced Arthritis ◽  
Autoimmune Encephalomyelitis ◽  
Novel Therapeutic ◽  
Experimental Autoimmune

Administration of Ti–O based nanomaterials ameliorated the clinical severity of experimental autoimmune encephalomyelitis and collagen induced arthritis, thus provide novel therapeutic approach for multiple sclerosis and rheumatoid arthritis.

scholarly journals Loss of HDAC11 ameliorates clinical symptoms in a multiple sclerosis mouse model

2018 ◽  
Vol 1 (5) ◽  
pp. e201800039 ◽  
Author(s):  
Lei Sun ◽  
Elphine Telles ◽  
Molly Karl ◽  
Fengdong Cheng ◽  
Noreen Luetteke ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Mouse Model ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Immune Cell ◽  
Demyelinating Disease ◽  
Demyelinating Diseases ◽  
Clinical Severity ◽  
Autoimmune Encephalomyelitis ◽  
Immune Mediated ◽  
Experimental Autoimmune

Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system (CNS). There is no known cure for MS, and currently available drugs for managing this disease are only effective early on and have many adverse side effects. Results from recent studies suggest that histone deacetylase (HDAC) inhibitors may be useful for the treatment of autoimmune and inflammatory diseases such as MS. However, the underlying mechanisms by which HDACs influence immune-mediated diseases such as MS are unclear. More importantly, the question of which specific HDAC(s) are suitable drug targets for the potential treatment of MS remains unanswered. Here, we investigate the functional role of HDAC11 in experimental autoimmune encephalomyelitis, a mouse model for MS. Our results indicate that the loss of HDAC11 in KO mice significantly reduces clinical severity and demyelination of the spinal cord in the post-acute phase of experimental autoimmune encephalomyelitis. The absence of HDAC11 leads to reduced immune cell infiltration into the CNS and decreased monocytes and myeloid DCs in the chronic progressive phase of the disease. Mechanistically, HDAC11 controls the expression of the pro-inflammatory chemokine C–C motif ligand 2 (CCL2) gene by enabling the binding of PU.1 transcription factor to the CCL2 promoter. Our results reveal a novel pathophysiological function for HDAC11 in CNS demyelinating diseases, and warrant further investigations into the potential use of HDAC11-specific inhibitors for the treatment of chronic progressive MS.

scholarly journals Protection of Fecal Microbiota Transplantation in a Mouse Model of Multiple Sclerosis

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Kanglan Li ◽  
Shouchao Wei ◽  
Li Hu ◽  
Xiaojian Yin ◽  
Yingren Mai ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Mouse Model ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Gut Microbiota ◽  
Effective Treatment ◽  
Therapeutic Approach ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

Given the growing evidence of a link between gut microbiota (GM) dysbiosis and multiple sclerosis (MS), fecal microbiota transplantation (FMT), aimed at rebuilding GM, has been proposed as a new therapeutic approach to MS treatment. To evaluate the viability of FMT for MS treatment and its impact on MS pathology, we tested FMT in mice with experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. We provide evidence that FMT can rectify altered GM to some extent with a therapeutic effect on EAE. We also found that FMT led to reduced activation of microglia and astrocytes and conferred protection on the blood-brain barrier (BBB), myelin, and axons in EAE. Taken together, our data suggest that FMT, as a GM-based therapy, has the potential to be an effective treatment for MS.

scholarly journals Transcranial Magnetic Stimulation Improves Muscle Involvement in Experimental Autoimmune Encephalomyelitis

2021 ◽  
Vol 22 (16) ◽  
pp. 8589
Author(s):  
Maria Angeles Peña-Toledo ◽  
Evelio Luque ◽  
Ignacio Ruz-Caracuel ◽  
Eduardo Agüera ◽  
Ignacio Jimena ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Skeletal Muscle ◽  
Transcranial Magnetic Stimulation ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Magnetic Stimulation ◽  
Clinical Severity ◽  
Autoimmune Encephalomyelitis ◽  
Muscle Involvement ◽  
Experimental Autoimmune

Skeletal muscle is affected in experimental autoimmune encephalomyelitis (EAE), which is a model of multiple sclerosis that produces changes including muscle atrophy; histological features of neurogenic involvement, and increased oxidative stress. In this study, we aimed to evaluate the therapeutic effects of transcranial magnetic stimulation (TMS) on the involvement of rat skeletal muscle and to compare them with those produced by natalizumab (NTZ). EAE was induced by injecting myelin oligodendrocyte glycoprotein (MOG) into Dark Agouti rats. Both treatments, NTZ and TMS, were implemented from day 15 to day 35. Clinical severity was studied, and after sacrifice, the soleus and extensor digitorum longus muscles were extracted for subsequent histological and biochemical analysis. The treatment with TMS and NTZ had a beneficial effect on muscle involvement in the EAE model. There was a clinical improvement in functional motor deficits, atrophy was attenuated, neurogenic muscle lesions were reduced, and the level of oxidative stress biomarkers was lower in both treatment groups. Compared to NTZ, the best response was obtained with TMS for all the parameters analyzed. The myoprotective effect of TMS was higher than that of NTZ. Thus, the use of TMS may be an effective strategy to reduce muscle involvement in multiple sclerosis.

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