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From celiac disease to coccidia infection and vice-versa: The polyQ peptide CXCR3-interaction axis
Martin A Lauxmann1,2, Diego S Vazquez3,4, Hanna M Schilbert5,6
1Institute for Biochemistry, Brandenburg Medical School (MHB) Theodor Fontane, Germany.
Insights
Celiac disease (CeD) involves zonulin upregulation, potentially triggered by coccidian parasites. Structural similarities between gliadin and parasite proteins suggest a novel environmental link to CeD pathogenesis and gluten-related disorders.
Area of Science:
- Gastroenterology
- Immunology
- Parasitology
Background:
- Zonulin regulates intercellular tight junctions and its upregulation is implicated in celiac disease (CeD).
- The immunogenic protein gliadin, specifically its polyQ fragment, binds to the CXCR3 receptor, increasing zonulin and intestinal permeability.
Purpose of the Study:
- To hypothesize a novel environmental trigger for celiac disease (CeD).
- To explore the structural similarities between gliadin and enteric coccidian parasite proteins.
- To propose coccidial infections as a potential cause of CeD.
Main Methods:
- Structural analysis comparing polyQ gliadin fragments with proteins from enteric coccidian parasites.
- Literature review on zonulin, gliadin, CXCR3, and coccidian infections.
Main Results:
- Identified structural similarities between the polyQ sequence in gliadin and proteins found in coccidian parasites.
- Described a potential novel host-parasite interaction pathway based on these structural similarities.
Conclusions:
- Coccidian infections may represent a novel environmental factor triggering celiac disease (CeD).
- This hypothesis offers a new perspective for coccidian research and potential preventive strategies for gluten-related disorders.
Abstract:
Zonulin is a physiological modulator of intercellular tight junctions, which upregulation is involved in several diseases like celiac disease (CeD). The polyQ gliadin fragment binds to the CXCR3 chemokine receptor that activates zonulin upregulation, leading to increased intestinal permeability in humans. Here, we report a general hypothesis based on the structural connection between the polyQ sequence of the immunogenic CeD protein, gliadin, and enteric coccidian parasites proteins. Firstly, a novel interaction pathway between the parasites and the host is described based on the structural similarities between polyQ gliadin fragments and the parasite proteins. Secondly, a potential connection between coccidial infections as a novel environmental trigger of CeD is hypothesized. Therefore, this report represents a promising breakthrough for coccidian research and points out the potential role of coccidian parasites as a novel trigger of CeD that might define a preventive strategy for gluten-related disorders in general. Also see the video abstract here: https://youtu.be/oMaQasStcFI.
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