BMSCs ameliorate septic coagulopathy through suppressing inflammation in cecal ligation and puncture induced sepsis
Autor: | Xiaogang Li, Zhen Zhou, Ziying Liu, Jingye Pan, Shunyao Xu, Xiaojun Pan, Fen Wang, Hao Li, Cong Wang, Yunbei Xiao, Yueyue Huang, Dequan Li |
---|---|
Rok vydání: | 2017 |
Předmět: |
Lipopolysaccharides
Male 0301 basic medicine Lipopolysaccharide Inflammation Punctures 030204 cardiovascular system & hematology Lung injury Biology Mesenchymal Stem Cell Transplantation Models Biological Proinflammatory cytokine Sepsis Pathogenesis 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Human Umbilical Vein Endothelial Cells medicine Coagulopathy Animals Humans Endothelial dysfunction Blood Coagulation Cecum Ligation Lung Macrophages Mesenchymal Stem Cells Cell Biology medicine.disease Mice Inbred C57BL 030104 developmental biology chemistry Immunology Inflammation Mediators medicine.symptom |
Zdroj: | Journal of Cell Science. |
ISSN: | 1477-9137 0021-9533 |
DOI: | 10.1242/jcs.211151 |
Popis: | Sepsis is an aggressive and life-threatening systemic inflammatory response with a high mortality. Inflammation and coagulation play crucial roles in the pathogenesis of sepsis in a mutually promoting manner. Unlike other single-target molecular therapies that have no obvious effects on clinical sepsis, the bone marrow stromal cell (BMSC) therapy offers a broader spectrum of activities ranging from immune and inflammation suppression to tissue regeneration. In this report, we demonstrated that BMSC injection attenuated the septic coagulopathy. It decreased the mortality, mitigated lung injury, and reduced the surge of proinflammatory factors in mice with sepsis induced by cecal ligation and puncture (CLP). In vitro cell model also revealed that co-culture with BMSCs reduced secretion of proinflammatory factors and injury of endothelial cells in response to lipopolysaccharides (LPS), an endotoxin of gram-negative bacteria. Together, our results demonstrated that BMSCs suppressed sepsis-induced inflammation, endothelial dysfunction, and defective coagulation. |
Databáze: | OpenAIRE |
Externí odkaz: |