Laboratory / cell studycited by the Tayebat archiveabstract only checked A-WHT-17 standard review

How gluten protein binds gut cells

Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3.

Overview

Lammers KM et al.. Gastroenterology 2008 · PMID 18485912 · DOI 10.1053/j.gastro.2008.03.023

Gliadin binds a receptor and increases permeability in mouse tissue.

Does the study support the specific claim? Unclear · Methodological quality: moderate

Original publication

Plain-language summary

Study explained simply
What did the researchers want to find out?

Mechanism

How was the study done?

Lab

What was actually found?

CXCR3 binding

What do the results mean in everyday life?

Lab mechanism

What are the study's limitations?

No clinical data; COI

What does it say about Elawady's specific claim?

Does not show harm in people

What can explicitly not be concluded from this study?

Clinical harm

Scientific in-depth review

1. Full reference

Authors
Lammers KM, Lu R, Brownley J, Lu B, Gerard C, Thomas K, Rallabhandi P, Shea-Donohue T, Tamiz A, Alkan S, Netzel-Arnett S, Antalis T, Vogel SN, Fasano A
Journal
Gastroenterology
Year
2008
Identifier
PMID 18485912 DOI 10.1053/j.gastro.2008.03.023 · PMC2653457
Verification
verified – PubMed E-utilities efetch, 2026-10-25
Retracted
no
Corrections
none
Extent checked
abstract only
Conflicts of interest and funding

COI: two authors (S.N.V., A.F.) have a financial relationship with Alba Therapeutics; NIH grants.

2. Research question

Molecular basis of gliadin-mucosa interaction

3. Study design and population

Study design
Laboratory / cell study – In vitro, mouse ex vivo, human biopsies
Population

Cell lines, mice, biopsies

Country

USA

Period

not stated

Sample size

not stated

4. Methods and endpoints

Exposure / intervention

Gliadin

Comparator

CXCR3-/- mice

Endpoints

Binding, zonulin, permeability

Statistical methods

Lab

5. Actual results

Results

Gliadin binds CXCR3; CXCR3 elevated in active coeliac disease and normalised on gluten-free diet; gliadin increased zonulin and permeability in wild-type but not CXCR3-/- mouse intestine.

Absolute risks

not applicable

Authors' conclusion

Gliadin binds CXCR3 and leads to MyD88-dependent zonulin release and permeability.

6. Strengths

  • Mechanistic

7. Weaknesses

  • Lab; COI

8. Risk of bias

Orienting tool
none applicable
Type of assessment
simplified assessment (abstract only)
Full formal assessment
no
Overall risk of bias
not assessable
Rationale

COI noted.

9. Assessment of the statistical interpretation

Not applicable.

10. Relevance to the specific claim

Mechanistic for C-WHT-09.

11. Independent contrary findings

I-WHT-07.

12. Transferability to Germany and Europe

13. Overall methodological judgement

Lab.

Multidimensional assessment
Multidimensional assessment
Authenticity of the sourceverified
Methodological qualitymoderate
Risk of biasnot assessable
Precision of resultsnot applicable
Directnessvery indirect
Reproducibilitypartly replicated
Consistency with the overall evidenceunknown
Regional transferabilityunknown
Adequacy of the interpretation (by the archive)not supported by the study

14. Open questions

15. Linked fact checks

Use by the Tayebat archive

Note: according to the archive, the studies were compiled by the archive operators. Whether Dr. Elawady himself cited this study is not established.

What the archive says about the study

Listed in bibliography only.

D. What does the archive derive from it?

Implies gluten harm.

E. Is this derivation scientifically justified?

Not justified for general population.

Adequacy of the interpretation (by the archive)
not supported by the study