David Artis
Weill Medical College of Cornell University, NY·Microbiology & Immunology
Food changes which microbes live in the gut, and those microbes release small molecules, called metabolites, that can travel through the bloodstream and tune the immune system far from the intestine. This work asks how dietary fiber reshapes that chemical output, and how the change steers type 2 inflammation, the arm of immunity that fights parasitic worms but also drives allergy.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Biochemistry
- Topics
microbiota
gut microbiome
microbial metabolites
- Grants
- 2 known grants, through May 2027
What they work on
- Determine which microbiota-derived metabolites induced by a high-fiber diet activate ILC2s (innate immune cells that trigger type 2 responses) and drive eosinophilia and type 2 inflammation that speeds worm expulsion in a mouse helminth model.
- Test with chemical and genetic approaches whether the microbiota's intrinsic bile acid metabolic pathway controls dietary-fiber-induced type 2 inflammation and protective immunity to helminth infection in mice.
- Identify the microbial metabolites and host metabolite receptors responsible for high-fiber-diet-induced type 2 inflammation, and measure their contribution to intestinal damage in mouse colitis models.
- Use a CRISPR-based microbial gene-editing technique to test directly which bacterial metabolic pathways allow a high-fiber diet to worsen intestinal inflammation.
- Relate microbial metabolite levels and the ILC2–eosinophil axis in samples from IBD patients to clinical and endoscopic measures of disease activity.
More about the research
In mice, the team found that a high-fiber diet shifts the microbiota (the gut's microbial community), markedly alters its metabolites, activates ILC2s (group 2 innate lymphoid cells, fast-acting immune cells that launch type 2 responses), and increases eosinophils, white blood cells that ILC2s control. Two projects follow this diet–microbe–ILC2 pathway into opposite outcomes: helpful expulsion of intestinal worms, and harmful inflammation of the colon.
Why it matters
Intestinal worm infections remain among the most neglected infectious diseases and carry a heavy global health and economic burden, while IBD drugs are expensive, fail in some patients, and carry risks including opportunistic infection, liver inflammation, pancreatitis and cancer. Mapping how diet-shaped microbial metabolites control type 2 immunity could suggest new ways to boost worm clearance and could give preclinical support for therapies, and better dietary advice, aimed at this pathway in IBD.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Elia D Tait Wojno
University of Washington, WA·Microbiology & Immunology
Test how Notch signaling inside basophils controls where they sit in the large intestine and how they contact CD4+ T cells during Trichuris muris worm infection, including a role for alpha4 integrin.
Ting Fu
University of Wisconsin-Madison, WI·Microbiology & Immunology
Determine how host- and microbe-derived bile acids generated during inflammation and tumor growth shape gut macrophages and their crosstalk with T cells and intestinal stem cells.
Pawel Kiela
University of Arizona, AZ·Microbiology & Immunology
Determine whether loss of NAD+ or excess PARylation by the enzyme PARP1 is the main driver of experimental colitis, using PARP1 knockout mice and drug inhibition.
The school
Weill Medical College of Cornell University: 35 labs on PI Pages, $1.6B a year on research, 59 research doctorates a year.
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