Molecular biology reports · 2025
Evaluating the influence of oleic and palmitic acids on inflammatory markers and gut barrier integrity in a celiac disease Caco-2 model.
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Ahmadi Behrooz, Nikzamir Abdolrahim, Sirati-Sabet Majid, Asri Nastaran, Rostami-Nejad Mohammad
Аннотация
BACKGROUND AND AIM: The fatty acid (FA) composition of the gluten-free diet (GFD) may affect mucosal responses in celiac disease (CeD). This study evaluated the effects of oleic acid (OA) and palmitic acid (PA) on gliadin-induced inflammation and barrier dysfunction using Caco-2 cells.
METHODS: Caco-2 cells were cultured under standard conditions and exposed to peptic-tryptic digested gliadin (PT-Gliadin) to induce a CeD-like response. Cells were treated with OA or PA under three conditions: co-treatment (with PT-Gliadin), pre-treatment (before PT-Gliadin), or post-treatment (after PT-Gliadin). Inflammatory gene expression (NF-κB, TNF-α, IL-6, IL-15) and tight junction markers (ZO-1, occludin) were quantified by qRT-PCR, while IL-6 and IL-15 secretion was measured by ELISA.
RESULTS: PT-Gliadin significantly increased inflammatory gene expression and cytokine secretion, while reducing ZO-1 and occludin levels (p < 0.05). OA co-treatment significantly suppressed NF-κB, TNF-α, IL-6, and IL-15 expression, lowered IL-6 and IL-15 secretion, and increased ZO-1 and occludin levels (p < 0.05). OA post-treatment also reduced NF-κB and IL-15 expression (p < 0.05) and diminished both IL-6 and IL-15 release (p < 0.05). Conversely, PA co-treatment elevated NF-κB, TNF-α, IL-6, and IL-15 expression (p < 0.05), increased IL-6 secretion (p < 0.05), and aggravated the loss of ZO-1 and occludin (p < 0.05). PA post-treatment similarly enhanced NF-κB, TNF-α, IL-6, and IL-15 expression (p < 0.05), increased IL-6 secretion (p < 0.05), and reduced occludin level (p < 0.05). Pre-treatment with either FA produced no significant effects.
CONCLUSION: OA mitigates, whereas PA exacerbates, gliadin-induced inflammation and barrier damage in Caco-2 cells. Modifying GFD fat composition to favor OA over PA may improve mucosal outcomes in CeD.
METHODS: Caco-2 cells were cultured under standard conditions and exposed to peptic-tryptic digested gliadin (PT-Gliadin) to induce a CeD-like response. Cells were treated with OA or PA under three conditions: co-treatment (with PT-Gliadin), pre-treatment (before PT-Gliadin), or post-treatment (after PT-Gliadin). Inflammatory gene expression (NF-κB, TNF-α, IL-6, IL-15) and tight junction markers (ZO-1, occludin) were quantified by qRT-PCR, while IL-6 and IL-15 secretion was measured by ELISA.
RESULTS: PT-Gliadin significantly increased inflammatory gene expression and cytokine secretion, while reducing ZO-1 and occludin levels (p < 0.05). OA co-treatment significantly suppressed NF-κB, TNF-α, IL-6, and IL-15 expression, lowered IL-6 and IL-15 secretion, and increased ZO-1 and occludin levels (p < 0.05). OA post-treatment also reduced NF-κB and IL-15 expression (p < 0.05) and diminished both IL-6 and IL-15 release (p < 0.05). Conversely, PA co-treatment elevated NF-κB, TNF-α, IL-6, and IL-15 expression (p < 0.05), increased IL-6 secretion (p < 0.05), and aggravated the loss of ZO-1 and occludin (p < 0.05). PA post-treatment similarly enhanced NF-κB, TNF-α, IL-6, and IL-15 expression (p < 0.05), increased IL-6 secretion (p < 0.05), and reduced occludin level (p < 0.05). Pre-treatment with either FA produced no significant effects.
CONCLUSION: OA mitigates, whereas PA exacerbates, gliadin-induced inflammation and barrier damage in Caco-2 cells. Modifying GFD fat composition to favor OA over PA may improve mucosal outcomes in CeD.