Evidence map›Paper›PMID 40982164›Full record

ArticleMolecular biology reports2025

Evaluating the influence of oleic and palmitic acids on inflammatory markers and gut barrier integrity in a celiac disease Caco-2 model.

Behrooz Ahmadi, Abdolrahim Nikzamir, Majid Sirati-Sabet, Nastaran Asri, Mohammad Rostami-Nejad

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Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 authors.

Behrooz AhmadiDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abdolrahim NikzamirDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Majid Sirati-SabetDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Nastaran AsriCeliac Disease and Gluten Related Disorders Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohammad Rostami-NejadCeliac Disease and Gluten Related Disorders Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran. m.rostamii@gmail.com.ORCID http://orcid.org/0000-0003-2495-1831

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimThe 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.

methodsCaco-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.

resultsPT-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.

conclusionOA 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.

Indexed as

Celiac DiseaseOleic AcidPalmitic AcidPalmitic AcidsBiomarkersCaco-2 CellsCytokinesDiet, Gluten-FreeGene Expression RegulationGliadinHumansInflammationInterleukin-6Intestinal MucosaNF-kappa BTight JunctionsBiomarkersCytokinesGliadinInterleukin-6NF-kappa BOleic AcidPalmitic AcidPalmitic AcidsTumor Necrosis Factor-alphaZonula Occludens-1 ProteinCeliac diseaseInflammatory responseOleic acidPalmitic acidTight junction integrity

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.