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Multiple sclerosis (MS) is a prevalent inflammatory neurodegenerative disease in young people, causing neurological abnormalities and impairment. To investigate a novel therapeutic agent for MS, we observed the impact of maresin 1 (MaR1) on disease progression in a well-known, relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE) mouse model. Treatment with MaR1 accelerated inflammation resolution, reduced neurological impairment, and delayed disease development by reducing immune cell infiltration (CD4+IL-17+ and CD4+IFNγ+) into the central nervous system (CNS).

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Targeting extracellular matrix components to attenuate microglia neuroinflammation: A study of fibulin-2 and CSPGs in a model of multiple sclerosis.

J Neuroimmunol

January 2025

Hotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta T2N 4N1, Canada; Department of Biology, University of Toronto Mississauga, Mississauga, Ontario L5L 1C6, Canada; Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada. Electronic address:

The extracellular matrix (ECM) plays an important role in the central nervous system (CNS), shaping tissue structure and functions as well as contributing to the pathology of chronic diseases such as multiple sclerosis (MS). ECM components, including fibulin-2 (FBLN2) and chondroitin sulfate proteoglycans (CSPGs), may impact neuroinflammation and remyelination. We investigated the capacity of FBLN2 to modulate immune responses and evaluated its interaction with CSPGs in experimental autoimmune encephalomyelitis (EAE), a common model for MS.

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The involvement of B lymphocytes in the pathogenesis of rheumatoid arthritis (RA) is well-established, with their early and aberrant activation being a crucial factor. However, the mechanisms underlying this abnormal activation in RA remain incompletely understood. In this study, we identified a significant reduction in MAPK4 expression in both RA patients and collagen-induced arthritis (CIA) mouse models, which correlates with disrupted B cell activation.

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Matching model with mechanism: Appropriate rodent models for studying various aspects of diabetes pathophysiology.

Methods Cell Biol

January 2025

School of Cardiovascular and Metabolic Medicine & Sciences, King's College London, London, United Kingdom. Electronic address:

Many rodent models are available for preclinical diabetes research making it a challenge for researchers to choose the most appropriate one for their experimental question. To aid in this, models have classically been categorized according to which type of diabetes they represent, and further into whether the model is induced, spontaneous or the result of genetic manipulation. This fails to capture the complexity of pathogenesis seen in diabetes in humans.

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Erianin alleviates autoimmune myocarditis by suppressing the M1 polarization of macrophages via the NF-κB/NLRP3 signaling pathway.

Eur J Pharmacol

January 2025

Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Hubei Key Laboratory of Biological Targeted Therapy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Hubei Provincial Engineering Research Center of Immunological Diagnosis and Therapy for Cardiovascular Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address:

Background: Myocarditis tends to lead to a poor prognosis, but there are no satisfactory preventive or therapeutic strategies. Erianin, a natural benzene compound, has been found to have antioxidant and anti-inflammatory effects. However, the effects of erianin on myocarditis remain unclear.

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