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Article ; Online: Induction of Sepsis Via Fibrin Clot Implantation.

Ghanta, Sailaja / Kwon, Min-Young / Perrella, Mark A

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2321, Page(s) 17–25

Abstract: Implantation of bacteria embedded in a fibrin clot allows for successful establishment of sepsis in preclinical models. This model allows the investigator to modulate the strain of bacteria as well as the bacterial load delivered. As it allows for a slow ...

Abstract	Implantation of bacteria embedded in a fibrin clot allows for successful establishment of sepsis in preclinical models. This model allows the investigator to modulate the strain of bacteria as well as the bacterial load delivered. As it allows for a slow release of standardized bacteria, the use of a fibrin clot model may be considered in studying the initial and later phases of sepsis and the host response to infection. Here we describe methods for performing the fibrin clot model of sepsis.
MeSH term(s)	Animals ; Bacteria/growth & development ; Disease Models, Animal ; Female ; Fibrin/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Sepsis/microbiology ; Thrombosis/microbiology
Chemical Substances	Fibrin (9001-31-4)
Language	English
Publishing date	2021-06-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1488-4_3
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Article: Bronchopulmonary Dysplasia: An Update of Current Pharmacologic Therapies and New Approaches.

Michael, Zoe / Spyropoulos, Fotios / Ghanta, Sailaja / Christou, Helen

Clinical medicine insights. Pediatrics

2018 Volume 12, Page(s) 1179556518817322

Abstract: Bronchopulmonary dysplasia (BPD) remains the most prevalent long-term morbidity of surviving extremely preterm infants and is associated with significant health care utilization in infancy and beyond. Recent advances in neonatal care have resulted in ... ...

Abstract	Bronchopulmonary dysplasia (BPD) remains the most prevalent long-term morbidity of surviving extremely preterm infants and is associated with significant health care utilization in infancy and beyond. Recent advances in neonatal care have resulted in improved survival of extremely low birth weight (ELBW) infants; however, the incidence of BPD has not been substantially impacted by novel interventions in this vulnerable population. The multifactorial cause of BPD requires a multi-pronged approach for prevention and treatment. New approaches in assisted ventilation, optimal nutrition, and pharmacologic interventions are currently being evaluated. The focus of this review is the current state of the evidence for pharmacotherapy in BPD. Promising future approaches in need of further study will also be reviewed.
Language	English
Publishing date	2018-12-11
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2579551-X
ISSN	1179-5565
ISSN	1179-5565
DOI	10.1177/1179556518817322
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Article ; Online: Mesenchymal Stromal Cell Therapy: Does the Source Matter?

Ghanta, Sailaja / Kwon, Min-Young / Rosas, Ivan O / Liu, Xiaoli / Perrella, Mark A

Critical care medicine

2018 Volume 46, Issue 2, Page(s) 343–345

MeSH term(s)	Adipose Tissue ; Bone Marrow ; Humans ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells ; Respiratory Distress Syndrome, Adult
Language	English
Publishing date	2018-02-14
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	197890-1
ISSN	1530-0293 ; 0090-3493
ISSN (online)	1530-0293
ISSN	0090-3493
DOI	10.1097/CCM.0000000000002894
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Article ; Online: Mesenchymal Stromal Cells Facilitate Neutrophil-Trained Immunity by Reprogramming Hematopoietic Stem Cells.

Ng, Julie / Marneth, Anna E / Griffith, Alec / Younger, Daniel / Ghanta, Sailaja / Jiao, Alan / Willis, Gareth / Han, Junwen / Imani, Jewel / Niu, Bailin / Keegan, Joshua W / Hancock, Brandon / Guo, Fei / Shi, Yang / Perrella, Mark A / Lederer, James A

Journal of innate immunity

2023 Volume 15, Issue 1, Page(s) 765–781

Abstract: Novel therapeutics are urgently needed to prevent opportunistic infections in immunocompromised individuals undergoing cancer treatments or other immune-suppressive therapies. Trained immunity is a promising strategy to reduce this burden of disease. We ... ...

Abstract	Novel therapeutics are urgently needed to prevent opportunistic infections in immunocompromised individuals undergoing cancer treatments or other immune-suppressive therapies. Trained immunity is a promising strategy to reduce this burden of disease. We previously demonstrated that mesenchymal stromal cells (MSCs) preconditioned with a class A CpG oligodeoxynucleotide (CpG-ODN), a Toll-like receptor 9 (TLR9) agonist, can augment emergency granulopoiesis in a murine model of neutropenic sepsis. Here, we used a chimeric mouse model to demonstrate that MSCs secrete paracrine factors that act on lineage-negative c-kit+ hematopoietic stem cells (HSCs), leaving them "poised" to enhance emergency granulopoiesis months after transplantation. Chimeric mice developed from HSCs exposed to conditioned media from MSCs and CpG-ODN-preconditioned MSCs showed significantly higher bacterial clearance and increased neutrophil granulopoiesis following lung infection than control mice. By Cleavage Under Targets and Release Using Nuclease (CUT&RUN) chromatin sequencing, we identified that MSC-conditioned media leaves H3K4me3 histone marks in HSCs at genes involved in myelopoiesis and in signaling persistence by the mTOR pathway. Both soluble factors and extracellular vesicles from MSCs mediated these effects on HSCs and proteomic analysis by mass spectrometry revealed soluble calreticulin as a potential mediator. In summary, this study demonstrates that trained immunity can be mediated by paracrine factors from MSCs to induce neutrophil-trained immunity by reprogramming HSCs for long-lasting functional changes in neutrophil-mediated antimicrobial immunity.
MeSH term(s)	Mice ; Animals ; Mesenchymal Stem Cell Transplantation ; Neutrophils ; Culture Media, Conditioned/metabolism ; Proteomics ; Trained Immunity ; Hematopoietic Stem Cells ; Mesenchymal Stem Cells/metabolism
Chemical Substances	Culture Media, Conditioned
Language	English
Publishing date	2023-10-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2454158-8
ISSN	1662-8128 ; 1662-811X
ISSN (online)	1662-8128
ISSN	1662-811X
DOI	10.1159/000533732
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Zs.A 6727: Show issues

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Article ; Online: Mesenchymal Stromal Cells Facilitate Neutrophil-Trained Immunity by Reprogramming Hematopoietic Stem Cells

Julie Ng / Anna E. Marneth / Alec Griffith / Daniel Younger / Sailaja Ghanta / Alan Jiao / Gareth Willis / Junwen Han / Jewel Imani / Bailin Niu / Joshua W. Keegan / Brandon Hancock / Fei Guo / Yang Shi / Mark A. Perrella / James A. Lederer

Journal of Innate Immunity, Vol 15, Iss 1, Pp 765-

2023 Volume 781

Abstract	Novel therapeutics are urgently needed to prevent opportunistic infections in immunocompromised individuals undergoing cancer treatments or other immune-suppressive therapies. Trained immunity is a promising strategy to reduce this burden of disease. We previously demonstrated that mesenchymal stromal cells (MSCs) preconditioned with a class A CpG oligodeoxynucleotide (CpG-ODN), a Toll-like receptor 9 (TLR9) agonist, can augment emergency granulopoiesis in a murine model of neutropenic sepsis. Here, we used a chimeric mouse model to demonstrate that MSCs secrete paracrine factors that act on lineage-negative c-kit+ hematopoietic stem cells (HSCs), leaving them “poised” to enhance emergency granulopoiesis months after transplantation. Chimeric mice developed from HSCs exposed to conditioned media from MSCs and CpG-ODN-preconditioned MSCs showed significantly higher bacterial clearance and increased neutrophil granulopoiesis following lung infection than control mice. By Cleavage Under Targets and Release Using Nuclease (CUT&RUN) chromatin sequencing, we identified that MSC-conditioned media leaves H3K4me3 histone marks in HSCs at genes involved in myelopoiesis and in signaling persistence by the mTOR pathway. Both soluble factors and extracellular vesicles from MSCs mediated these effects on HSCs and proteomic analysis by mass spectrometry revealed soluble calreticulin as a potential mediator. In summary, this study demonstrates that trained immunity can be mediated by paracrine factors from MSCs to induce neutrophil-trained immunity by reprogramming HSCs for long-lasting functional changes in neutrophil-mediated antimicrobial immunity.
Keywords	trained immunity ; epigenetics ; hematopoietic stem cells ; neutrophils ; toll-like receptor 9 ; Medicine ; R ; Internal medicine ; RC31-1245
Subject code	571
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	Karger Publishers
Document type	Article ; Online
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Article ; Online: Mesenchymal stromal cells expressing a dominant-negative high mobility group A1 transgene exhibit improved function during sepsis.

Kwon, Min-Young / Ghanta, Sailaja / Ng, Julie / Castano, Ana P / Han, Junwen / Ith, Bonna / Lederer, James A / El-Chemaly, Souheil / Chung, Su Wol / Liu, Xiaoli / Perrella, Mark A

Journal of leukocyte biology

2021 Volume 110, Issue 4, Page(s) 711–722

Abstract: High mobility group (HMG)A proteins are nonhistone chromatin proteins that bind to the minor groove of DNA, interact with transcriptional machinery, and facilitate DNA-directed nuclear processes. HMGA1 has been shown to regulate genes involved with ... ...

Abstract	High mobility group (HMG)A proteins are nonhistone chromatin proteins that bind to the minor groove of DNA, interact with transcriptional machinery, and facilitate DNA-directed nuclear processes. HMGA1 has been shown to regulate genes involved with systemic inflammatory processes. We hypothesized that HMGA1 is important in the function of mesenchymal stromal cells (MSCs), which are known to modulate inflammatory responses due to sepsis. To study this process, we harvested MSCs from transgenic (Tg) mice expressing a dominant-negative (dn) form of HMGA1 in mesenchymal cells. MSCs harvested from Tg mice contained the dnHMGA1 transgene, and transgene expression did not change endogenous HMGA1 levels. Immunophenotyping of the cells, along with trilineage differentiation revealed no striking differences between Tg and wild-type (WT) MSCs. However, Tg MSCs growth was decreased compared with WT MSCs, although Tg MSCs were more resistant to oxidative stress-induced death and expressed less IL-6. Tg MSCs administered after the onset of Escherichia coli-induced sepsis maintained their ability to improve survival when given in a single dose, in contrast with WT MSCs. This survival benefit of Tg MSCs was associated with less tissue cell death, and also a reduction in tissue neutrophil infiltration and expression of neutrophil chemokines. Finally, Tg MSCs promoted bacterial clearance and enhanced neutrophil phagocytosis, in part through their increased expression of stromal cell-derived factor-1 compared with WT MSCs. Taken together, these data demonstrate that expression of dnHMGA1 in MSCs provides a functional advantage of the cells when administered during bacterial sepsis.
MeSH term(s)	Adipocytes/cytology ; Animals ; Cell Death ; Cell Proliferation ; Cell Survival ; Chemokine CXCL12/biosynthesis ; Escherichia coli/physiology ; Genes, Dominant ; HMGA1a Protein/genetics ; HMGA1a Protein/metabolism ; Inflammation/pathology ; Interleukin-6/biosynthesis ; Male ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells/metabolism ; Mice, Inbred C57BL ; Mice, Transgenic ; Neutrophil Infiltration ; Neutrophils/metabolism ; Oxidative Stress ; Phagocytosis ; Sepsis/microbiology ; Sepsis/pathology ; Sepsis/therapy ; Transgenes ; Mice
Chemical Substances	Chemokine CXCL12 ; Interleukin-6 ; HMGA1a Protein (124544-67-8)
Language	English
Publishing date	2021-01-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1002/JLB.4A0720-424R
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Zs.A 603: Show issues

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Article ; Online: An update on pharmacologic approaches to bronchopulmonary dysplasia.

Ghanta, Sailaja / Leeman, Kristen Tropea / Christou, Helen

Seminars in perinatology

2013 Volume 37, Issue 2, Page(s) 115–123

Abstract: Bronchopulmonary dysplasia (BPD) is the most prevalent long-term morbidity in surviving extremely preterm infants and is linked to increased risk of reactive airways disease, pulmonary hypertension, post-neonatal mortality, and adverse neurodevelopmental ...

Abstract	Bronchopulmonary dysplasia (BPD) is the most prevalent long-term morbidity in surviving extremely preterm infants and is linked to increased risk of reactive airways disease, pulmonary hypertension, post-neonatal mortality, and adverse neurodevelopmental outcomes. BPD affects approximately 20% of premature newborns, and up to 60% of premature infants born before completing 26 weeks of gestation. It is characterized by the need for assisted ventilation and/or supplemental oxygen at 36 weeks postmenstrual age. Approaches to prevention and treatment of BPD have evolved with improved understanding of its pathogenesis. This review will focus on recent advancements and detail current research in pharmacotherapy for BPD. The evidence for both current and potential future experimental therapies will be reviewed in detail. As our understanding of the complex and multifactorial pathophysiology of BPD changes, research into these current and future approaches must continue to evolve.
MeSH term(s)	Adrenal Cortex Hormones/therapeutic use ; Bronchodilator Agents/therapeutic use ; Bronchopulmonary Dysplasia/drug therapy ; Bronchopulmonary Dysplasia/prevention & control ; Diuretics/therapeutic use ; Humans ; Infant, Low Birth Weight ; Infant, Newborn ; Infant, Premature ; Infant, Very Low Birth Weight ; Pulmonary Surfactants/therapeutic use ; Vitamin A/therapeutic use ; Vitamins/therapeutic use ; Xanthines/therapeutic use
Chemical Substances	Adrenal Cortex Hormones ; Bronchodilator Agents ; Diuretics ; Pulmonary Surfactants ; Vitamins ; Xanthines ; Vitamin A (11103-57-4)
Language	English
Publishing date	2013-03-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	752403-1
ISSN	1558-075X ; 0146-0005
ISSN (online)	1558-075X
ISSN	0146-0005
DOI	10.1053/j.semperi.2013.01.008
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Article ; Online: Augmenting emergency granulopoiesis with CpG conditioned mesenchymal stromal cells in murine neutropenic sepsis.

Ng, Julie / Guo, Fei / Marneth, Anna E / Ghanta, Sailaja / Kwon, Min-Young / Keegan, Joshua / Liu, Xiaoli / Wright, Kyle T / Kamaz, Baransel / Cahill, Laura A / Mullally, Ann / Perrella, Mark A / Lederer, James A

Blood advances

2020 Volume 4, Issue 19, Page(s) 4965–4979

Abstract: Patients with immune deficiencies from cancers and associated treatments represent a growing population within the intensive care unit with increased risk of morbidity and mortality from sepsis. Mesenchymal stromal cells (MSCs) are an integral part of ... ...

Abstract	Patients with immune deficiencies from cancers and associated treatments represent a growing population within the intensive care unit with increased risk of morbidity and mortality from sepsis. Mesenchymal stromal cells (MSCs) are an integral part of the hematopoietic niche and express toll-like receptors, making them candidate cells to sense and translate pathogenic signals into an innate immune response. In this study, we demonstrate that MSCs administered therapeutically in a murine model of radiation-associated neutropenia have dual actions to confer a survival benefit in Pseudomonas aeruginosa pneumo-sepsis that is not from improved bacterial clearance. First, MSCs augment the neutrophil response to infection, an effect that is enhanced when MSCs are preconditioned with CpG oligodeoxynucleotide, a toll-like receptor 9 agonist. Using cytometry by time of flight, we identified proliferating neutrophils (Ly6GlowKi-67+) as the main expanded cell population within the bone marrow. Further analysis revealed that CpG-MSCs expand a lineage restricted progenitor population (Lin-Sca1+C-kit+CD150-CD48+) in the bone marrow, which corresponded to a doubling in the myeloid proliferation and differentiation potential in response to infection compared with control. Despite increased neutrophils, no reduction in organ bacterial count was observed between experimental groups. However, the second effect exerted by CpG-MSCs is to attenuate organ damage, particularly in the lungs. Neutrophils obtained from irradiated mice and cocultured with CpG-MSCs had decreased neutrophil extracellular trap formation, which was associated with decreased citrullinated H3 staining in the lungs of mice given CpG-MSCs in vivo. Thus, this preclinical study provides evidence for the therapeutic potential of MSCs in neutropenic sepsis.
MeSH term(s)	Animals ; Hematopoiesis ; Humans ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells ; Mice ; Neutropenia/therapy ; Sepsis/therapy
Language	English
Publishing date	2020-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2020002556
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Zs.A 7153: Show issues

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Article ; Online: Mesenchymal stromal cell-derived syndecan-2 regulates the immune response during sepsis to foster bacterial clearance and resolution of inflammation.

Han, Junwen / Shi, Yuanyuan / Willis, Gareth / Imani, Jewel / Kwon, Min-Young / Li, Gu / Ayaub, Ehab / Ghanta, Sailaja / Ng, Julie / Hwang, Narae / Tsoyi, Konstantin / El-Chemaly, Souheil / Kourembanas, Stella / Mitsialis, S Alex / Rosas, Ivan O / Liu, Xiaoli / Perrella, Mark A

The FEBS journal

2021 Volume 289, Issue 2, Page(s) 417–435

Abstract: Sepsis is a life-threatening process related to a dysregulated host response to an underlying infection, which results in organ dysfunction and poor outcomes. Therapeutic strategies using mesenchymal stromal cells (MSCs) are under investigation for ... ...

Abstract	Sepsis is a life-threatening process related to a dysregulated host response to an underlying infection, which results in organ dysfunction and poor outcomes. Therapeutic strategies using mesenchymal stromal cells (MSCs) are under investigation for sepsis, with efforts to improve cellular utility. Syndecan (SDC) proteins are transmembrane proteoglycans involved with cellular signaling events including tissue repair and modulating inflammation. Bone marrow-derived human MSCs express syndecan-2 (SDC2) at a level higher than other SDC family members; thus, we explored SDC2 in MSC function. Administration of human MSCs silenced for SDC2 in experimental sepsis resulted in decreased bacterial clearance, and increased tissue injury and mortality compared with wild-type MSCs. These findings were associated with a loss of resolution of inflammation in the peritoneal cavity, and higher levels of proinflammatory mediators in organs. MSCs silenced for SDC2 had a decreased ability to promote phagocytosis of apoptotic neutrophils by macrophages in the peritoneum, and also a diminished capability to convert macrophages from a proinflammatory to a proresolution phenotype via cellular or paracrine actions. Extracellular vesicles are a paracrine effector of MSCs that may contribute to resolution of inflammation, and their production was dramatically reduced in SDC2-silenced human MSCs. Collectively, these data demonstrate the importance of SDC2 for cellular and paracrine function of human MSCs during sepsis.
MeSH term(s)	Animals ; Cell Polarity/genetics ; Cell Polarity/immunology ; Disease Models, Animal ; Extracellular Vesicles/genetics ; Extracellular Vesicles/immunology ; Extracellular Vesicles/microbiology ; Gene Expression Regulation, Developmental/genetics ; Gene Silencing ; Humans ; Immunity/genetics ; Inflammation/genetics ; Inflammation/microbiology ; Inflammation/pathology ; Inflammation/therapy ; Macrophages/immunology ; Macrophages/microbiology ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells/metabolism ; Mice ; Neutrophils/immunology ; Neutrophils/microbiology ; Paracrine Communication/genetics ; Phagocytosis/genetics ; Sepsis/genetics ; Sepsis/microbiology ; Sepsis/pathology ; Sepsis/therapy ; Syndecan-2/genetics
Chemical Substances	SDC2 protein, human ; Syndecan-2 (149769-25-5)
Language	English
Publishing date	2021-08-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16154
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Article ; Online: Expression of Stromal Cell-Derived Factor-1 by Mesenchymal Stromal Cells Impacts Neutrophil Function During Sepsis.

Kwon, Min-Young / Ghanta, Sailaja / Ng, Julie / Tsoyi, Konstantin / Lederer, James A / Bronson, Roderick T / El-Chemaly, Souheil / Chung, Su Wol / Liu, Xiaoli / Perrella, Mark A

Critical care medicine

2020 Volume 48, Issue 5, Page(s) e409–e417

Abstract: Objectives: Sepsis results in organ dysfunction caused by a dysregulated host response, in part related to the immune response of a severe infection. Mesenchymal stromal cells are known to modulate the immune response, and expression of stromal cell- ... ...

Abstract	Objectives: Sepsis results in organ dysfunction caused by a dysregulated host response, in part related to the immune response of a severe infection. Mesenchymal stromal cells are known to modulate the immune response, and expression of stromal cell-derived factor-1 regulates mobilization of neutrophils from the bone marrow. We are investigating the importance of stromal cell-derived factor-1 in mesenchymal stromal cells and its role in promoting neutrophil function after the onset of cecal ligation and puncture-induced sepsis. Stromal cell-derived factor-1 expression was silenced in mesenchymal stromal cells, compared with the control scrambled construct mesenchymal stromal cells. Design: Animal study and cell culture. Setting: Laboratory investigation. Subjects: BALB/c mice. Interventions: Polymicrobial sepsis was induced by cecal ligation and puncture. shSCR mesenchymal stromal cells and shSDF-1 mesenchymal stromal cells were delivered by tail vein injections to septic mice. The mice were assessed for survival, bacterial clearance, and the inflammatory response during sepsis in each of the groups. Mesenchymal stromal cells were also assessed for their ability to promote bacterial phagocytosis by neutrophils. Measurements and main results: Injection of shSCR mesenchymal stromal cells after the onset of sepsis led to an increase in mouse survival (70%) at 7 days, whereas survival of mice receiving shSDF-1 mesenchymal stromal cells was significantly diminished (33%). The loss of survival benefit in mice receiving shSDF-1 mesenchymal stromal cells was associated with less efficient bacterial clearance compared with shSCR mesenchymal stromal cells. Although shSCR mesenchymal stromal cells, or their conditioned medium, were able to increase neutrophil phagocytosis of bacteria, this effect was significantly blunted with shSDF-1 mesenchymal stromal cells. Assessment of peritoneal inflammation revealed that neutrophils were significantly increased and more immature in septic mice receiving shSDF-1 mesenchymal stromal cells. This response was associated with hypocellularity and increased neutrophil death in the bone marrow of mice receiving shSDF-1 mesenchymal stromal cells. Conclusions: Expression of stromal cell-derived factor-1 in mesenchymal stromal cells enhances neutrophil function with increased phagocytosis, more efficient clearance of bacteria, and bone marrow protection from depletion of cellular reserves during sepsis.
MeSH term(s)	Animals ; Chemokine CXCL12/pharmacology ; Disease Models, Animal ; Mesenchymal Stem Cells/physiology ; Mice, Inbred BALB C ; Neutrophils/metabolism ; Phagocytosis/drug effects ; Sepsis/mortality ; Sepsis/therapy
Chemical Substances	Chemokine CXCL12
Language	English
Publishing date	2020-03-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	197890-1
ISSN	1530-0293 ; 0090-3493
ISSN (online)	1530-0293
ISSN	0090-3493
DOI	10.1097/CCM.0000000000004244
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