Evidence map›Paper›PMID 40333150›Full record

ArticlePathogens (Basel, Switzerland)2025

Tartaric Acid Exacerbates DSS-Induced Colitis by Promoting Eosinophilic Inflammation via IL-13 and IL-5Rα Upregulation.

Bushra Riaz, Hye-Myung Ryu, Bunsoon Choi, Seonghyang Sohn

Abstract read
In one paragraph

Article in Pathogens (Basel, Switzerland), 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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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Bushra RiazDepartment of Biomedical Sciences, Ajou University School of Medicine, Suwon 16499, Republic of Korea.ORCID 0000-0001-5754-1324
Hye-Myung RyuDepartment of Microbiology, Ajou University School of Medicine, Suwon 16499, Republic of Korea.ORCID 0000-0003-0349-9815
Bunsoon ChoiInstitute of Medical Science, Ajou University School of Medicine, Suwon 16499, Republic of Korea.
Seonghyang SohnDepartment of Biomedical Sciences, Ajou University School of Medicine, Suwon 16499, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eosinophils are granulocytes involved in the effector phase of type 2 T cell immune responses, which are elevated in inflammatory conditions like ulcerative colitis (UC) and other allergic diseases. UC is a chronic inflammatory colon disease, marked by excessive eosinophil infiltration and elevated Th2 cytokines, which contribute to mucosal inflammation and tissue damage. Dietary factors, including certain organic acids, can influence UC progression by modulating gut immune responses. This research is the first to explore the dose-dependent effects of tartaric acid (TA), a naturally occurring organic acid widely used in the food industry, on eosinophil activation and Th2 cytokine response in both normal mice and a dextran sulfate sodium (DSS)-induced colitis model. Normal mice were treated with TA at varying doses (5 µg, 25 µg, and 50 µg/mouse/day), while colitis mice received 50 µg TA. Eosinophil activation markers (CD11b+, SiglecF+, and CCR3+), Th2 cytokines (IL-4, IL-13, and IL-31), and IL-17 were assessed in peripheral blood leukocytes, lymph nodes, and splenocytes using flow cytometry. Additionally, mRNA expression levels of eosinophil-associated chemokines and cytokines in the splenocytes were quantified with real-time qPCR. Our results demonstrate a dose-dependent effect of TA, with the highest dose (50 µg) significantly increasing eosinophil activation markers, Th2 cytokines, IL-17, and mRNA expression of SiglecF, CCL11, and toll-like receptor 4 in normal mice. In colitis mice, treatment with 50 µg TA showed marked increases in IL-13 levels compared to those of untreated colitis mice, reflecting increased eosinophil recruitment to inflamed tissues. Moreover, mRNA expression of IL-5Rα was elevated in normal mice and colitis mice administered with TA. These results suggest that TA enhances eosinophil proliferation, the upregulation of their regulatory molecules, and Th2 immune profiles, potentially worsening the severity of colitis.

Indexed as

ColitisEosinophilsInflammationInterleukin-13TartratesAnimalsCytokinesDextran SulfateDisease Models, AnimalMaleMiceTh2 CellsUp-RegulationCytokinesDextran SulfateInterleukin-13tartaric acidTartratescolitiseosinophilsmouse modeltartaric acidTh2 cytokines

Identifiers

PMID40333150
PMCPMC12030069

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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.