AI Article Synopsis
- Crosstalk between gastric epithelial cells and stromal fibroblasts plays a crucial role in cell growth, differentiation, and transformation within the gastric mucosa.
- The bacterium Helicobacter pylori, known for causing gastric issues, activates the NF-κB transcription factor which triggers a pro-inflammatory response and promotes cell survival during infection.
- Findings indicate that H. pylori infection reduces cell death in gastric cancer cells by increasing A20 expression, a negative regulator of cell death pathways, showcasing the protective role of gastric fibroblasts during such infections.
Article Abstract
Crosstalk within the gastric epithelium, which is closely in contact with stromal fibroblasts in the gastric mucosa, has a pivotal impact in proliferation, differentiation and transformation of the gastric epithelium. The human pathogen Helicobacter pylori colonises the gastric epithelium and represents a risk factor for gastric pathophysiology. Infection of H. pylori induces the activation of the transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), which is involved in the pro-inflammatory response but also in cell survival. In co-cultures with human gastric fibroblasts (HGF), we found that apoptotic cell death is reduced in the polarised human gastric cancer cell line NCI-N87 or in gastric mucosoids during H. pylori infection. Interestingly, suppression of apoptotic cell death in NCI-N87 cells involved an enhanced A20 expression regulated by NF-κB activity in response to H. pylori infection. Moreover, A20 acts as an important negative regulator of caspase-8 activity, which was suppressed in NCI-N87 cells during co-culture with gastric fibroblasts. Our results provide evidence for NF-κB-dependent regulation of apoptotic cell death in cellular crosstalk and highlight the protective role of gastric fibroblasts in gastric epithelial cell death during H. pylori infection.
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| http://dx.doi.org/10.1016/j.bbamcr.2022.119364 | DOI Listing |
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