Advances in Mesenchymal Stem Cell Research in Sepsis

Wannemuehler, Todd J.; Manukyan, Mariuxi C.; Brewster, Benjamin D.; Rouch, Joshua D.; Poynter, Jeffrey A.; Wang, Yue; Meldrum, Daniel R.

doi:10.1016/j.jss.2011.09.053

Cited by 60 publications

(55 citation statements)

References 130 publications

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“…Interest in investigating the therapeutic effect of MSCs on experimental models of sepsis emerged recently, and is based on their immunomodulatory properties [58] . A description of the therapeutic effects of MSCs in experimental small animal models of sepsis and the mechanisms involved are described in the following sections.…”

Section: Msc In Experimental Models Of Sepsismentioning

confidence: 99%

“…Two limitations of sepsis models compared to human disease are the timing of disease progression (the progression to multiorgan failure and death occurs in hours to days in most animal models, whereas in human sepsis this occurs in days to weeks) and lack of supportive therapeutic intervention (i.e., intubation and mechanical ventilation, fluid therapy), in particular in small animal models. Therefore, extrapolation of efficacy results obtained in small sepsis animal models to the human disease has to be made with caution [58,59] . The toxemia models involve the administration by intraperitoneal or intravenous injection of a bacterial toxin.…”

Section: Experimental Models Of Sepsismentioning

confidence: 99%

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Mesenchymal stem cells as a therapeutic tool to treat sepsis

Lombardo¹

2015

WJSC

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Sepsis is a clinical syndrome caused by a deregulated host response to an infection. Sepsis is the most frequent cause of death in hospitalized patients. Although knowledge of the pathogenesis of sepsis has increased substantially during the last decades, attempts to design effective and specific therapies targeting components of the derailed host response have failed. Therefore, there is a dramatic need for new and mechanistically alternative therapies to treat this syndrome. Based on their immunomodulatory properties, adult mesenchymal stem or stromal cells (MSCs) can be a novel therapeutic tool to treat sepsis. Indeed, MSCs reduce mortality in experimental models of sepsis by modulating the deregulated inflammatory response against bacteria through the regulation of multiple inflammatory networks, the reprogramming of macrophages and neutrophils towards a more antiinflammatory phenotype and the release of antimicrobial peptides. This report will review the current knowledge on the effects of MSC treatment in preclinical experimental small animal models of sepsis.

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Section: Msc In Experimental Models Of Sepsismentioning

confidence: 99%

Section: Experimental Models Of Sepsismentioning

confidence: 99%

Mesenchymal stem cells as a therapeutic tool to treat sepsis

Lombardo¹

2015

WJSC

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“…Despite decades of clinical trials and improvement in antibiotic and supportive care, sepsis remains a challenging life-threatening disease in critically ill patients and the leading cause of morbidity and mortality in ICU patients 258 . In the United States, sepsis is responsible for more than 200,000 patient deaths and utilizes US$17 billion per year 259,260 .…”

Section: Mesenchymal Stem Cells In Sepsis and Multiple Organ Dysfunctmentioning

confidence: 99%

Cell-based Therapy for Acute Organ Injury

et al. 2014

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Critically ill patients often suffer from multiple organ failures involving lung, kidney, liver or brain. Genomic, proteomic and metabolomic approaches highlight common injury mechanisms leading to acute organ failure. This underlines the need to focus on therapeutic strategies affecting multiple injury pathways. The use of adult stem cells such as mesenchymal stem or stromal cells (MSC) may represent a promising new therapeutic approach as increasing evidence shows that MSC can exert protective effects following injury through the release of pro-mitotic, anti-apoptotic, anti-inflammatory and immunomodulatory soluble factors. Furthermore, they can mitigate metabolomic and oxidative stress imbalance. In this work, we review the biological capabilities of MSC and the results of clinical trials using MSC as therapy in acute organ injuries. Although preliminary results are encouraging, more studies concerning safety and efficacy of MSC therapy are needed to determine their optimal clinical use.

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“…Our results collectively suggest that the salutary effects of E2 on hepatic injury following hemorrhagic shock and resuscitation are in part mediated through an estrogen-receptor-related p38 MAPK-dependent HO-1 upregulation. hemorrhagic shock; estrogen; liver injury; p38 MAPK; HO-1; estrogen receptor antagonist DESPITE NUMEROUS ADVANCES in intensive care medicine, profound shock, sepsis and severe damage leading to multiple organ failure remain the major causes of death in the injured host (25,28,29,35). The liver has been shown to play an important role in the development of delayed organ dysfunction following traumatic damage and massive blood loss (18).…”

mentioning

confidence: 99%

“…DESPITE NUMEROUS ADVANCES in intensive care medicine, profound shock, sepsis and severe damage leading to multiple organ failure remain the major causes of death in the injured host (25,28,29,35). The liver has been shown to play an important role in the development of delayed organ dysfunction following traumatic damage and massive blood loss (18).…”

mentioning

confidence: 99%

Role of p38 MAPK pathway in 17β-estradiol-mediated attenuation of hemorrhagic shock-induced hepatic injury

Chen

Chiang

Kuo

et al. 2015

Journal of Applied Physiology

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Although 17β-estradiol (E2) treatment following hemorrhagic shock or ischemic reperfusion prevents organs from dysfunction and injury, the precise mechanism remains unknown. We hypothesize that the E2-mediated attenuation of liver injury following hemorrhagic shock and fluid resuscitation occurs via the p38 mitogen-activated protein kinase (MAPK)-dependent heme oxygenase (HO)-1 pathway. After a 5-cm midline laparotomy, male rats underwent hemorrhagic shock (mean blood pressure ∼40 mmHg for 90 min) followed by fluid resuscitation. At the onset of resuscitation, rats were treated with vehicle, E2 (1 mg/kg) alone, or E2 plus p38 MAPK inhibitor SB-203580 (2 mg/kg), HO-1 inhibitor chromium mesoporphyrin-IX chloride (2.5 mg/kg) or estrogen receptor antagonist ICI 182,780 (3 mg/kg). At 2 h after hemorrhagic shock and fluid resuscitation, the liver injury markers were significantly increased compared with sham-operated control. Hemorrhagic shock resulted in a significant decrease in p38 MAPK phosphorylation compared with the shams. Administration of E2 following hemorrhagic shock normalized liver p38 MAPK phosphorylation, further increased HO-1 expression, and reduced cleaved caspase-3 levels. Coadministration of SB-203580 abolished the E2-mediated attenuation of the shock-induced liver injury markers. In addition, administration of chromium mesoporphyrin-IX chloride or ICI 182,780 abolished E2-mediated increases in liver HO-1 expression or p38 MAPK activation following hemorrhagic shock. Our results collectively suggest that the salutary effects of E2 on hepatic injury following hemorrhagic shock and resuscitation are in part mediated through an estrogen-receptor-related p38 MAPK-dependent HO-1 upregulation.

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Advances in Mesenchymal Stem Cell Research in Sepsis

Cited by 60 publications

References 130 publications

Mesenchymal stem cells as a therapeutic tool to treat sepsis

Mesenchymal stem cells as a therapeutic tool to treat sepsis

Cell-based Therapy for Acute Organ Injury

Role of p38 MAPK pathway in 17β-estradiol-mediated attenuation of hemorrhagic shock-induced hepatic injury

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