Bone marrow-derived mononuclear cells (BMMNCs) secrete anti-inflammatory mediators that protect against acute
inflammation. Current evidence suggests that BMMNC
transplantation can reduce acute tissue injury caused by systemic
inflammation and lung dysfunction. This study evaluated the role of BMMNCs in reducing systemic inflammatory responses to vascular endothelial injury in
sepsis. Bone marrow cells were harvested from the tibias and femurs of 12-week-old male Wistar rats; BMMNCs were separated by density centrifugation. Additional rats underwent cecal
ligation and
puncture (CLP) or similar
sham surgery. BMMNCs were injected intravenously 30 min after CLP. The
Sham and CLP Control groups were administered PBS. The 7-day survival rate improved markedly in the CLP-BMMNC group compared with that in the Control group. BMMNCs markedly suppressed the serum levels of pro-inflammatory mediators such as
tumor necrosis factor-alpha,
interleukin-6, and
histone H3 at 3, 6, and 12 h after CLP. In the CLP-BMMNC group, the serum levels of
syndecan-1, the main component of the vascular endothelial glycocalyx layer, were notably lower than those in the Control group 6 h after CLP. Histological analysis revealed improvement of morphological damages in the CLP-BMMNC group. Ultrastructural analysis revealed that the glycocalyx structure was maintained and the continuity of the vascular endothelial glycocalyx layer was preserved in the BMMNC group, compared with the case for the Control group at 6 and 12 h. Therefore, BMMNC
transplantation may provide reduced systemic
inflammation and endothelial glycocalyx damage, dramatically improving the survival of rats. These findings provide insights into formulating potential therapeutic strategies against
sepsis.