Lipopolysaccharide (LPS) extracted from Bacteroides vulgatus effectively prevents LPS extracted from Escherichia coli from inducing epithelial‑mesenchymal transition

Pathological epithelial-mesenchymal transition (EMT) has been shown to fulfill a key role in the development and progression of a variety of lung diseases. It has been demonstrated that the inflammatory microenvironment is a decisive factor in inducing pathological EMT. Hexacylated lipopolysaccharide (LPS) [or proacylated lipopolysaccharide (P-LPS), which functions as proinflammatory lipopolysaccharide] is one of the most effective Toll-like receptor 4 (TLR4) agonists. Furthermore, the pentacylated and tetracylated form of lipopolysaccharide (or A-LPS, which functions as anti-inflammatory lipopolysaccharide) has been shown to elicit competitive antagonistic effects against the pro-inflammatory activity of P-LPS. At present, it remains unclear whether LPS extracted from Bacteroides vulgatus (BV-LPS) can prevent LPS extracted from Escherichia coli (EC-LPS) from inducing pathological EMT. In the present study, A549 cells and C57BL/6 mice lung tissue were both induced by EC-LPS (P-LPS) and BV-LPS (A-LPS), either alone or in combination. The anticipated anti-inflammatory effects of BV-LPS were analyzed by examining the lung coefficient, lung pathology, A549 cell morphology and expression levels both of the inflammatory cytokines, IL-1β, IL-6 and TNF-α and of the EMT signature proteins, epithelial cadherin (E-cadherin), α-smooth muscle actin (α-SMA) and vimentin. In addition, the expression levels of TLR4, bone morphogenic protein and activin membrane-bound inhibitor (BAMBI) and Snail were detected and the possible mechanism underlying how BV-LPS may prevent EC-LPS-induced EMT was analyzed. The results obtained showed that the morphology of the A549 cells was significantly polarized, the lung index was significantly increased, the alveolar structure was collapsed and the expression levels of IL-1β, IL-6, TNF-α, α-SMA, vimentin, TLR4 and Snail in both lung tissue and A549 cells were significantly increased, whereas those of E-cadherin and BAMBI were significantly decreased. Treatment with BV-LPS in combination with EC-LPS was found to reverse these changes. In conclusion, the present study demonstrated that BV-LPS is able to effectively prevent EC-LPS-induced EMT in A549 cells and in mouse lung tissue and furthermore, the underlying mechanism may be associated with inhibition of the TLR4/BAMBI/Snail signaling pathway.