Cord blood rescues stroke-induced changes in splenocyte phenotype and function

Vendrame, Martina; Gemma, Carmelina; Pennypacker, Keith R.; Bickford, Paula C.; Sanberg, Cyndy D.; Sanberg, Paul R.; Willing, Alison E.

doi:10.1016/j.expneurol.2006.03.017

Cited by 222 publications

(236 citation statements)

References 45 publications

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“…Both clinical and animal studies have demonstrated transient reduction in spleen size following stroke, which has been attributed to the poststroke deployment of splenocytes, including monocytes [25,[83][84][85]. The extent of spleen atrophy is associated with the severity of stroke-induced brain injury, leading to the view that the spleen plays a contributory role in stroke pathology [26,86]. Increased apoptosis in the spleen, albeit controversial (see Kim et al [25]), and cell release from the spleen are related to reduced spleen size [26].…”

Section: Monocytes and Monocyte-derived Macrophagesmentioning

confidence: 99%

Microglia and Monocyte-Derived Macrophages in Stroke

2016

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Historically, the brain has been considered an immune-privileged organ separated from the peripheral immune system by the blood-brain barrier. However, immune responses do occur in the brain in neurological conditions in which the integrity of the blood-brain barrier is compromised, exposing the brain to peripheral antigens and endogenous danger signals. While most of the associated pathological processes occur in the central nervous system, it is now clear that peripheral immune cells, especially mononuclear phagocytes, that infiltrate into the injury site play a key role in modulating the progression of primary brain injury development. As inflammation is a necessary and critical component for the subsequent injury resolution process, understanding the contribution of mononuclear phagocytes on the regulation of inflammatory responses may provide novel approaches for potential therapies. Furthermore, predisposed comorbid conditions at the time of stroke cause the alteration of stroke-induced immune and inflammatory responses and subsequently influence stroke outcome. In this review, we summarize a role for microglia and monocytes/macrophages in acute ischemic stroke in the context of normal and metabolically compromised conditions.

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Section: Monocytes and Monocyte-derived Macrophagesmentioning

confidence: 99%

Microglia and Monocyte-Derived Macrophages in Stroke

2016

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“…Collectively, these studies indicate that intravenous delivery of many types of cell therapies change the splenic response after stroke thereby altering inflammatory cell trafficking to the brain and the overall peripheral immune response [31,60]. As a result, secondary injury within the brain is significantly attenuated, which, ultimately, may facilitate brain repair.…”

Section: Targeting the Spleen As A Therapeutic Strategymentioning

confidence: 99%

“…Various types of cell populations have been isolated from umbilical cord for applications in stroke. Numerous studies have shown neuroprotective effects of human umbilical cord blood stem cells comparable with that of bone marrow stromal cells [1,[28][29][30][31][32][33]. Human adipose tissue is also known to contain pluripotent stromal cells and serves as a well explored alternative to bone marrow and umbilical cells [34][35][36][37][38][39].…”

Section: Human Umbilical Cord Blood Stem Cellsmentioning

confidence: 99%

“…Vendrame et al [31] reported more than 10 years ago that the intravenous administration of umbilical cord cells leads to their migration to the spleen where they restore splenic mass and T cells back to the levels comparable in rats without stroke. These cells also downregulated proinflammatory gene expression and upregulated anti-inflammatory gene expression.…”

Section: Targeting the Spleen As A Therapeutic Strategymentioning

confidence: 99%

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Is Immunomodulation a Principal Mechanism Underlying How Cell-Based Therapies Enhance Stroke Recovery?

Satani

Savitz

2016

Neurotherapeutics

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Inflammation within the brain and in peripheral tissues contributes to brain injury following ischemic stroke. Therapeutic modulation of the inflammatory response has been actively pursued as a novel stroke treatment approach for decades, without success. In recent years, extensive studies support the high potential for cell-based therapies to become a new treatment modality for stroke and other neurological disorders. In this review, we explore different types of cellular therapies and discuss how they modulate central and peripheral inflammatory processes after stroke. Apart from identifying potential targets for cell therapy, we also discuss paracrine and immunomodulatory mechanisms of cell therapy.

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“…In the ischemic brain parenchyma of rats subjected to stroke, HUCBC treatment significantly decreases infiltration of granulocytes and monocytes, and decreases astroglial and microglial activation 47. HUCBC treatment after stroke can also modulate peripheral immune responses and rescue stroke induced gross spleen size and CD8+ T‐cell number decrease which correlates with the extent of ischemic injury to the brain 48.…”

Section: Cell‐based Therapies and Exosome Therapy For Diabetic Strokementioning

confidence: 99%

Cell-Based and Exosome Therapy in Diabetic Stroke

Venkat

Chopp

Chen

2018

Stem Cells Translational Medicine

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SummaryStroke is a global health concern and it is imperative that therapeutic strategies with wide treatment time frames be developed to improve neurological outcome in patients. Patients with diabetes mellitus who suffer a stroke have worse neurological outcomes and long‐term functional recovery than nondiabetic stroke patients. Diabetes induced vascular damage and enhanced inflammatory milieu likely contributes to worse post stroke outcomes. Diabetic stroke patients have an aggravated pathological cascade, and treatments that benefit nondiabetic stroke patients do not necessarily translate to diabetic stroke patients. Therefore, there is a critical need to develop therapeutics for stroke specifically in the diabetic population. Stem cell based therapy for stroke is an emerging treatment option with wide therapeutic time window. Cell‐based therapies for stroke promote endogenous central nervous system repair and neurorestorative mechanisms such as angiogenesis, neurogenesis, vascular remodeling, white matter remodeling, and also modulate inflammatory and immune responses at the local and systemic level. Emerging evidence suggests that exosomes and their cargo microRNA mediate cell therapy derived neurorestorative effects. Exosomes are small vesicles containing protein and RNA characteristic of its parent cell. Exosomes are transported by biological fluids and facilitate communication between neighboring and remote cells. MicroRNAs, a class of naturally occurring, small noncoding RNA sequences, contained within exosomes can regulate recipient cell's signaling pathways and alter protein expression either acting alone or in concert with other microRNAs. In this perspective article, we summarize current knowledge and highlight the promising future of cell based and exosome therapy for stroke and specifically for diabetic stroke. stem cells translational medicine 2018;7:451–455

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Cord blood rescues stroke-induced changes in splenocyte phenotype and function

Cited by 222 publications

References 45 publications

Microglia and Monocyte-Derived Macrophages in Stroke

Microglia and Monocyte-Derived Macrophages in Stroke

Is Immunomodulation a Principal Mechanism Underlying How Cell-Based Therapies Enhance Stroke Recovery?

Cell-Based and Exosome Therapy in Diabetic Stroke

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