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Healthy infants harbor intestinal bacteria that protect against food allergy.

Taylor Feehley | Catherine H Plunkett | Riyue Bao | Sung Min Choi Hong | Elliot Culleen | Pedro Belda-Ferre | Evelyn Campbell | Rosita Aitoro | Rita Nocerino | Lorella Paparo | Jorge Andrade | Dionysios A Antonopoulos | Roberto Berni Canani | Cathryn R Nagler
Nature medicine | 2019

There has been a striking generational increase in life-threatening food allergies in Westernized societies1,2. One hypothesis to explain this rising prevalence is that twenty-first century lifestyle practices, including misuse of antibiotics, dietary changes, and higher rates of Caesarean birth and formula feeding have altered intestinal bacterial communities; early-life alterations may be particularly detrimental3,4. To better understand how commensal bacteria regulate food allergy in humans, we colonized germ-free mice with feces from healthy or cow's milk allergic (CMA) infants5. We found that germ-free mice colonized with bacteria from healthy, but not CMA, infants were protected against anaphylactic responses to a cow's milk allergen. Differences in bacterial composition separated the healthy and CMA populations in both the human donors and the colonized mice. Healthy and CMA colonized mice also exhibited unique transcriptome signatures in the ileal epithelium. Correlation of ileal bacteria with genes upregulated in the ileum of healthy or CMA colonized mice identified a clostridial species, Anaerostipes caccae, that protected against an allergic response to food. Our findings demonstrate that intestinal bacteria are critical for regulating allergic responses to dietary antigens and suggest that interventions that modulate bacterial communities may be therapeutically relevant for food allergy.

Pubmed ID: 30643289

Research resources used in this publication

None found

Antibodies used in this publication

None found

Associated grants

  • Agency: NCATS NIH HHS, United States
    Id: UL1 TR000430
  • Agency: NIDDK NIH HHS, United States
    Id: P30 DK042086
  • Agency: NCI NIH HHS, United States
    Id: P30 CA014599
  • Agency: NIAID NIH HHS, United States
    Id: R56 AI134923
  • Agency: NIGMS NIH HHS, United States
    Id: R25 GM109439
  • Agency: NIAID NIH HHS, United States
    Id: T32 AI007090
  • Agency: NCATS NIH HHS, United States
    Id: UL1 TR002389
  • Agency: NIAID NIH HHS, United States
    Id: R01 AI106302

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PRISM (tool)

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THIS RESOURCE IS NO LONGER IN SERVICE. Documented on May 5,2022.Tool that predicts interactions between transcription factors and their regulated genes from binding motifs. Understanding vertebrate development requires unraveling the cis-regulatory architecture of gene regulation. PRISM provides accurate genome-wide computational predictions of transcription factor binding sites for the human and mouse genomes, and integrates the predictions with GREAT to provide functional biological context. Together, accurate computational binding site prediction and GREAT produce for each transcription factor: 1. putative binding sites, 2. putative target genes, 3. putative biological roles of the transcription factor, and 4. putative cis-regulatory elements through which the factor regulates each target in each functional role.

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