Anti-inflammatory effect of lactobacilli bacteria on HepG2 cells is through cross-regulation of TLR4 and NOD2 signalling

Abstract

Pathogen peptidoglycans are detected via host’s innate immune system. This course of action is executed by nucleotide-binding oligomerization domain (NOD) proteins, which have been identified inducing inflammation through nuclear factor-kappa B (NF-κB). Excessive stimulation of liver cells by endotoxin leds to severe inflammatory symptoms. In this research, seven strains of lactobacilli bacteria were prior processed into crude cell wall extracts, followed by testing if crude cell wall extracts could lessen pro-inflammatory processes launched by lipopolysaccharides. The results showed lactobacilli bacteria activated NOD2 expression in mild degrees, and did not lead to serious inflammation. Prior exposure of HepG2 cells to lactobacilli bacteria rendered them desensitized to subsequent LPS challenge. The mechanism by which lactobacilli bacteria attenuated inflammation might be because of the fact that lactobacilli bacteria induced interleukin-10, suppressor of cytokine signalling 1/3 and peroxisome proliferator-activated receptors alpha via NOD2-NF-κB pathway, and then cross-regulated Toll-like receptor 4 (TLR4) downstream signal transduction.

Keywords

• Cell injury
• Lactobacilli bacteria
• LPS
• Mechanism of action
• PPARα
• Suppressor of cytokine signalling