Cytokine · 2025
Inflammation in gastric epithelium associated with infection of Helicobacter pylori is induced by inhibited PPARγ pathway: the key role of TLRs/NF-κB axis.
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Mao Jianna, Shen Yuhou, Qi Hongyang
Аннотация
BACKGROUND: Helicobacter pylori infection is a major risk factor for the development of peptic ulcer disease and associated cancers, posing a significant public health concern. Peroxisome proliferator-activated receptor gamma (PPARγ) has been implicated in mucosal healing and may modulate H. pylori-induced gastric injury. In this study, we investigated the role of PPARγ in the progression of H. pylori-induced gastric ulceration.
METHOD: The potential association between PPARγ level and H. pylori infection rate was firstly analyzed with clinical samples. Then the effects of PPARγ activation on H. pylori-induced inflammation in human gastric epithelial cells (HGECs) were evaluated using CCK-8 assays for cell viability and immunofluorescence for inflammatory markers. The expression of PPARγ downstream effectors, including TLRs/NF-κB axis was also detected.
RESULTS: Clinical analysis revealed that H. pylori infection significantly increased the risk of gastric ulcer development. PPARγ levels were inversely correlated with H. pylori infection rate and with the concentrations of IL-6, IL-1β, and TNF-α. In HGECs, lipopolysaccharide (LPS) treatment induced abnormal cell viability and heightened inflammatory responses, both of which were attenuated by the PPARγ agonist pioglitazone. Pioglitazone selectively promoted apoptosis in LPS-treated cells. At the molecular level, LPS increased expression of TLR2, TLR4, and TLR5, leading to NF-κB pathway activation; PPARγ activation suppressed both TLR expression and NF-κB signaling, coinciding with reduced cytokine release.
CONCLUSIONS: The current study demonstrates that PPARγ activation exerts anti-H. pylori effects during gastric ulcer progression by inhibiting the TLR/NF-κB signaling pathway.
METHOD: The potential association between PPARγ level and H. pylori infection rate was firstly analyzed with clinical samples. Then the effects of PPARγ activation on H. pylori-induced inflammation in human gastric epithelial cells (HGECs) were evaluated using CCK-8 assays for cell viability and immunofluorescence for inflammatory markers. The expression of PPARγ downstream effectors, including TLRs/NF-κB axis was also detected.
RESULTS: Clinical analysis revealed that H. pylori infection significantly increased the risk of gastric ulcer development. PPARγ levels were inversely correlated with H. pylori infection rate and with the concentrations of IL-6, IL-1β, and TNF-α. In HGECs, lipopolysaccharide (LPS) treatment induced abnormal cell viability and heightened inflammatory responses, both of which were attenuated by the PPARγ agonist pioglitazone. Pioglitazone selectively promoted apoptosis in LPS-treated cells. At the molecular level, LPS increased expression of TLR2, TLR4, and TLR5, leading to NF-κB pathway activation; PPARγ activation suppressed both TLR expression and NF-κB signaling, coinciding with reduced cytokine release.
CONCLUSIONS: The current study demonstrates that PPARγ activation exerts anti-H. pylori effects during gastric ulcer progression by inhibiting the TLR/NF-κB signaling pathway.