hWJMSCs inhibit inflammation and apoptosis in an ARDS cell model.

UNLABELLED

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.

OBJECTIVE

This research evaluated the potential of human Wharton's jelly MSCs (hWJMSCs) to inhibit inflammation and apoptosis in lipopolysaccharide (LPS)-induced rat lung cells (L2).

METHODS

hWJMSC 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.

RESULTS

hWJMSCs 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.

CONCLUSION

Co-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.