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Background: Biomarker for prognosis of stroke is urgently needed for the management of acute ischemic stroke (AIS) patients.
Objective: To evaluate the course of inflammatory cytokines in AIS patients and its comparison with inter-alfa trypsin inhibitor heavy chain 4 (ITIH4) and outcome after AIS.
Materials And Methods: A panel of 12 inflammatory cytokines and ITIH4 were estimated in serial blood samples collected at admission, 24 h, 48 h, 72 h, 144 h and at discharge of AIS patients (n = 5).
Results: Out of the 12 cytokines, only interleukin (IL)-2, tumor necrosis factor-alfa (TNF-α), IL-10, IL-6, IL-1B and IL-8 were in the measurable range of the kit (10 pg/mL). We found high IL-2 at admission, which decreased (P < 0.05) in the follow-up samples. TNF-α initially increases (P < 0.05) at 24 h followed by gradual decrease (P < 0.05) after 72 h. IL-10 decreases initially (P < 0.05) till 72 h as compared with its level at admission and then increases (P < 0.05) after 144 h. Similarly, ITIH4 was down-regulated in the early 72 h followed by further increase with improvement of the patient. ITIH4 correlates with IL-10 and computed tomography scan infarct volume. Serum IL-6, IL-1B and IL-8 increased in the AIS patients, but did not show any pattern.
Conclusions: Serial measurement of IL-10, IL-2 and TNF-α and ITIH4 may be useful for the follow-up of clinical outcome after AIS.
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http://dx.doi.org/10.4103/0972-2327.99707 | DOI Listing |
Haematologica
September 2025
Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD,.
Immunotherapies, including cell therapies, are effective anti-cancer agents. However, cellular product persistence can be limiting with short functional duration of activity contributing to disease relapse. A variety of manufacturing protocols are used to generate therapeutic engineered T-cells; these differ in techniques used for T-cell isolation, activation, genetic modification, and other methodology.
View Article and Find Full Text PDFJ Neurochem
September 2025
Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Microglia, the resident immune cells of the central nervous system (CNS), are involved in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease (AD), Dementia with Lewy Bodies (DLB), and Parkinson's disease (PD). 14-3-3 proteins act as molecular hubs to regulate protein-protein interactions, which are involved in numerous cellular functions, including cellular signaling, protein folding, and apoptosis. We previously revealed decreased 14-3-3 levels in the brains of human subjects with neurodegenerative diseases.
View Article and Find Full Text PDFCNS Neurosci Ther
September 2025
Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Aims: Sustained neuroinflammation following ischemic stroke impedes post-injury tissue repairment and neurological functional recovery. Developing innovative therapeutic strategies that simultaneously suppress detrimental inflammatory cascades and facilitate neurorestorative processes is critical for improving long-term rehabilitation outcomes.
Methods: We employed a microglia depletion-repopulation paradigm by administering PLX5622 for 7 days post-ischemia; followed by a 7-day withdrawal period to allow microglia repopulation.
Schizophr Bull
September 2025
Department of Psychiatry, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Background And Hypothesis: Schizophrenia is linked to hippocampal dysfunction and microglial inflammatory activation. Our prior clinical findings revealed significantly reduced transient receptor potential vanilloid 1 (TRPV1) expression in both first-episode and recurrent schizophrenia patients, with levels inversely correlating with symptom severity, implicating TRPV1 dysfunction in disease progression. Preclinical maternal separation (MS) models recapitulate schizophrenia-like behavioral and synaptic deficits, paralleled by hippocampal microglial TRPV1 downregulation.
View Article and Find Full Text PDFAdv Healthc Mater
September 2025
State Key Laboratory of Southwestern Chinese Medicine Resources, College of Modern Chinese Medicine Industry, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by joint inflammation, damage, and disability. Activated fibroblast-like synoviocytes (FLSs), abundant in RA synovium, crucially facilitate disease progression. These activated FLSs drive RA pathogenesis by upregulating adhesion molecules, proinflammatory cytokines, chemokines, and major histocompatibility complex class II (MHC-II).
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