Objective: Mesenchymal stem cells (MSCs) were an emergent tool to prevent acute lung injury (ALI) and its complications. We attempted to isolate, culture, and characterize chicken bone marrow-derived mesenchymal stem cells (BM-MSCs), investigate whether BM-MSCs protect against lipopolysaccharide (LPS)-induced ALI, and explore the related mechanisms. Methods: Ninety-six male ICR (6 wks old) mice were divided into three groups: Con, LPS, and LPS + MSC. Mice in the LPS and Ex+LPS groups received 5 mg/kg LPS intratracheally to induce ALI. Histopathological micrographs showed morphological changes in the lung, heart, liver, kidney, and aorta. Lung permeability, bronchoalveolar lavage fluid (BALF) cell counts, oxidative stress parameters, and inflammatory cytokine levels in the BALF, plasma, and lung tissue were detected. Furthermore, gene expression levels for Toll-Like Receptor 4 (TRL4) and myeloid differentiation factor (Mdy88) were measured. Besides, a survival analysis was performed in sixty male ICR mice. Results: BM-MSCs administration significantly increased the survival rate and decreased the histopathological severity of LPS-induced lung, liver, kidney, and aortic injury. BM-MSC administration improved LPS-induced pulmonary inflammation, systemic inflammation, and oxidative stress injury. BM-MSC administration reduced the infiltration of neutrophils in lung, liver, kidney, and heart tissues. In addition, BM-MSC administration reduced TRL4 and Mdy88 mRNA expression in mice with ALI. Conclusions: Chicken BM-MSCs improved LPS-induced ALI and liver, kidney, heart, and aortic injury. Chicken BM-MSCs improved LPS-induced ALI, in part through TLR4/Myd88 signaling and inhibition of inflammation and oxidative stress injury. BM-MSCs improved LPS-induced pulmonary fibrosis via suppressing TGF-β and MMP-9. BM-MSCs reduced neutrophil content via suppressing CXCL-1, IL-8, and TNF-α.

Purpose: In the present study, we attempted to investigate whether aerobic exercise (AE) could prevent sepsis and its complications and explored the related mechanisms. Methods: Forty ICR mice were divided into four groups: Control (Con), Lipopolysaccharide (LPS), Exercise (Ex), and Exercise + LPS (Ex + LPS) groups. Ex and Ex + LPS mice were performed with low-intensity AE for 4 weeks. LPS and Ex + LPS mice received 5 mg/kg LPS intraperitoneally for induction of sepsis. Histopathological micrographs showed the organ injury. This study examined the effects of AE on LPS-induced changes in systemic inflammation, pulmonary inflammation, lung permeability, oxidative stress-related indicators in the lung, blood glucose levels, plasma lactate levels, and plasma high-mobility group box 1 (HMGB1) levels, and bronchoalveolar lavage fluid (BALF) cell count. Sixty mice were used to perform survival rate analysis. Results: AE improved survival rates, MODS, and aortic injury in mice with sepsis. AE decreased LPS-induced oxidative stress injury in lung tissue. AE reduced the infiltration of neutrophils in the lung, liver, kidney, and heart tissues. AE suppressed CXCL-1, CXCL-8, IL-6, and TNF-α mRNA expression but activated IL-1RN, IL-10, Sirt-1, and Nrf-2 mRNA expression in the lung. AE decreased the serum levels of lactate and HMGB1 but increased blood glucose levels during sepsis. Conclusions: AE improves sepsis-associated lung, liver, kidney, heart, and aortic injury and death. AE modulates the inflammatory-anti-inflammatory and oxidative-antioxidative balance in the lung. AE, which can regulate the Warburg effect and impair LPS-induced lactate and HMGB1 release, is a novel therapeutic strategy for sepsis targeting aerobic glycolysis.