Future microbiology · 2026
Targeting PPARγ-NF-κB: (+)-catechin reverses Clostridioides difficile toxin A-induced intestinal barrier dysfunction.
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Li Shufeng, Luan Yibo, Li Zongmin, Lu Yuting, Lai Dingyuan, Chen Kai
Аннотация
BACKGROUND: Clostridioides difficile toxin A (TcdA) is a key factor in antibiotic-associated intestinal epithelial injury. (+)-Catechin (CC) exhibits anti-inflammatory and antioxidant properties, but its role in protecting intestinal epithelial barrier function during TcdA exposure remains unclear.
METHODS: Human colon epithelial Caco-2 cells were treated with TcdA to induce barrier dysfunction, followed by CC at varying concentrations. Barrier integrity was assessed using trans-epithelial electrical resistance (TEER), Lucifer yellow paracellular flux, and lactate dehydrogenase (LDH) release. The involvement of peroxisome proliferator-activated receptor gamma (PPARγ) and nuclear factor kappa B (NF-κB) signaling was evaluated using short hairpin RNA (shRNA)-mediated PPARγ knockdown.
RESULTS: TcdA treatment disrupted Caco-2 barrier function, indicated by decreased TEER, increased Lucifer yellow flux, and elevated LDH release. TcdA treatment also reduced PPARγ expression and was associated with increased activation of the NF-κB signaling pathway. CC treatment significantly alleviated these effects in a concentration-dependent manner, with 100 μg/mL showing optimal protection. PPARγ knockdown partially attenuated the protective effects of CC and diminished its inhibitory effect on NF-κB activation, suggesting that PPARγ contributes to the barrier-protective role of CC.
CONCLUSION: CC attenuates TcdA-induced intestinal epithelial barrier dysfunction and is associated with modulation of the PPARγ-NF-κB signaling pathway.
METHODS: Human colon epithelial Caco-2 cells were treated with TcdA to induce barrier dysfunction, followed by CC at varying concentrations. Barrier integrity was assessed using trans-epithelial electrical resistance (TEER), Lucifer yellow paracellular flux, and lactate dehydrogenase (LDH) release. The involvement of peroxisome proliferator-activated receptor gamma (PPARγ) and nuclear factor kappa B (NF-κB) signaling was evaluated using short hairpin RNA (shRNA)-mediated PPARγ knockdown.
RESULTS: TcdA treatment disrupted Caco-2 barrier function, indicated by decreased TEER, increased Lucifer yellow flux, and elevated LDH release. TcdA treatment also reduced PPARγ expression and was associated with increased activation of the NF-κB signaling pathway. CC treatment significantly alleviated these effects in a concentration-dependent manner, with 100 μg/mL showing optimal protection. PPARγ knockdown partially attenuated the protective effects of CC and diminished its inhibitory effect on NF-κB activation, suggesting that PPARγ contributes to the barrier-protective role of CC.
CONCLUSION: CC attenuates TcdA-induced intestinal epithelial barrier dysfunction and is associated with modulation of the PPARγ-NF-κB signaling pathway.