HWJMSCs inhibit inflammation and apoptosis in an ARDS cell model

Abstract

Acute respiratory distress syndrome (ARDS) is a type of lung failure caused by fluids and hypoxemia. Mesenchymal stem cells (MSCs) have been shown to decrease levels of pro-inflammatory mediators and inflammatory cells. These cells have anti-inflammatory, anti-apoptotic, and anti-microbial activity, and protect against lung injury. ObjectiveThis research evaluated the potential of human Wharton's jelly MSCs (hWJMSCs) to inhibit inflammation and apoptosis in lipopolysaccharide (LPS)-induced rat lung cells (L2). MethodshWJMSC treatment in LPS-induced rat lung cells was performed with 1:1, 1:5, 1:10, or 1:25 ratios of hWJMSCs to L2 cells. The gene expression of angiotensin-converting enzyme-2 (ACE-2), receptor for advanced glycation end products (RAGE), nuclear factor kappa B (NFκB), and C-X-C motif chemokine ligand-9 (CXCL-9) was quantified with RT-PCR, and the levels of C-reactive protein (CRP), interleukin-12 (IL-12), and tumor necrosis factor-alpha (TNF-α) were measured with ELISA. ResultshWJMSCs increased ACE-2 gene expression, and decreased CXCL-9, NFκB, and RAGE gene expression. The treatment also suppressed CRP, TNF-α, and IL-12 levels, and increased the percentage of live cells, but decreased the percentages of necrotic cells and apoptotic cells in inflammatory rat lung cells, which served as an ARDS cell model. ConclusionCo-culture of hWJMSCs and L2 cells mitigated inflammation through increasing ACE-2 gene expression, and decreasing CXCL-9, NFκB, and RAGE gene expression; decreasing TNF-α and CRP protein levels; and decreasing necrosis, and early and late apoptosis. A co-culture ratio of 1:1 was most effective.