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Floyd School of Medicine

Floyd School of Medicine Student and Faculty Combine for Study on Gluten Sensitivity

Kay and C. Edward Floyd, M.D. School of Medicine Ph.D. student Ryan Ball joined with Pathology, Microbiology and Immunology Associate Professor Jason Kubinak, Ph.D. as first and senior authors on a study published in "Gut Microbes" a journal that publishes research on intestinal microbiota. They studied how selective IgA deficiency (sIgAD) and gluten sensitivity are linked.

Abstract

Selective IgA deficiency (sIgAD) is the most common type of immune system disorder and has long been associated with increased risk of developing gut inflammation caused by the ingestion of dietary gluten (also known as gluten sensitivity). How sIgAD and gluten sensitivity are linked has been unclear. To address this, researchers studied mice that could not make IgA and compared them with normal mice. They found that when the IgA-deficient mice ate gluten, the lining of their small intestine became damaged and inflamed. However, when these mice were fed a gluten-free diet, this damage did not occur. Importantly, the researchers found that the gut microbiota of normal mice did not change in the presence of dietary gluten, while the gut microbiota of sIgAD mice changed considerably.

To see if these changes caused gluten sensitivity, the researchers transferred whole gut bacterial communities as well as a single species of bacteria called Streptococcus lutetiensis into germ-free mice. Both approaches caused similar intestinal problems in germfree mice, showing that gut bacteria are important drivers of gluten sensitivity. These results suggest that a lack of IgA in the gut allows dietary inputs like gluten to cause blooms of pro-inflammatory bacterial species in the small intestine.


IgA deficiency reveals a microbiota-dependent pathway to gluten sensitivity.

Ball RAW, Mohammed AD, Jolly A, Johnson K, Sklenicka S, Kucherina M, Peacock T, Liu E, Hogan KM, Baird M, Peña MMO, Nagarkatti P, Nagarkatti M, Kubinak JL.

Gut Microbes. IMPACT FACTOR: 15.3 2026 Dec 31;18(1):2724175. doi: 10.1080/19490976.2026.2724175. Epub 2026 Sep 18.

PMID: 42758655     


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