Inflammatory response involved in cartilage degeneration induced by T-2 toxin: systematic review

The aim of our study was to explore the role of inflammatory factors in degenerated articular cartilage exposure to T-2 toxin. The search strings were performed in PubMed database, CBM (Chinese Biomedical Literature Database), EMBASE, Web of Science, Wanfang database and CNKI (Chinese Journal Full Text Database). The random effect model was adopted to analyze the inflammatory markers, interleukin-6 (IL-6), interleukin-1β (IL-1β) ,and tumor necrosis factor-α (TNF-α), of cartilage degeneration induced by T-2 toxin. The differentially expressed genes of cartilage degeneration by T-2 toxin were identified, and the molecular mechanism was observed by Protein-Protein Interaction (PPI) network analysis, Cytoscape, as well as GO functional annotation (GO) and KEGG pathway enrichment analysis (KEGG). his study identified 40 chondrocytes related inflammatory genes from 13 published studies. Among them, the 26 genes were included in the PPI analysis. Gene network analysis revealed that inflammation, extracellular matrix degradation, and apoptosis were involved in the damaged chondrocytes exposed to T-2 toxin. Additionally, IL-6 was identified as a key gene in the Cytoscape analysis. GO and KEGG further demonstrated that these differentially expressed genes were mainly enriched in inflammation- and apoptosis-related pathways, which were closely associated with chondrocyte degeneration processes.Moreover, the levels of IL-6, TNF-α, and IL-1β were significantly higher in the T-2 toxin group than those in control group. Specifically, the significant differences were observed in serum levels of IL-6 (SMD = 3.80, 95% CI: 1.65-5.95, P_heter=0.000) and TNF-α (SMD = 1.76, 95% CI: 0.22-3.30, P_heter=0.001), whereas IL-1β did not show statistical significance (SMD = 0.77, 95% CI: -0.70-2.24, P_heter=0.032). T-2 toxin exacerbates cartilage degeneration by activating the release of inflammatory factors (IL-6), which cause an imbalance in cartilage matrix metabolism and cell death.