Defective humoral immunity disrupts bile acid homeostasis which promotes inflammatory disease of the small bowel

Ahmed Dawood Mohammed, Zahraa Mohammed, Mary M. Roland, Ioulia Chatzistamou, Amy Jolly, Lillian M. Schoettmer, Mireya Arroyo, Khadija Kakar, Yuan Tian, Andrew Patterson, Mitzi Nagarkatti, Prakash Nagarkatti and Jason L. Kubinak ()
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Ahmed Dawood Mohammed: University of South Carolina School of Medicine Department of Pathology, Microbiology
Zahraa Mohammed: University of South Carolina School of Medicine Department of Pathology, Microbiology
Mary M. Roland: University of South Carolina School of Medicine Department of Pathology, Microbiology
Ioulia Chatzistamou: University of South Carolina School of Medicine Department of Pathology, Microbiology
Amy Jolly: University of South Carolina School of Medicine Department of Pathology, Microbiology
Lillian M. Schoettmer: University of South Carolina School of Medicine Department of Pathology, Microbiology
Mireya Arroyo: University of South Carolina School of Medicine Department of Pathology, Microbiology
Khadija Kakar: University of South Carolina School of Medicine Department of Pathology, Microbiology
Yuan Tian: Pennsylvania State University Department of Veterinary and Biomedical Sciences
Andrew Patterson: Pennsylvania State University Department of Veterinary and Biomedical Sciences
Mitzi Nagarkatti: University of South Carolina School of Medicine Department of Pathology, Microbiology
Prakash Nagarkatti: University of South Carolina School of Medicine Department of Pathology, Microbiology
Jason L. Kubinak: University of South Carolina School of Medicine Department of Pathology, Microbiology

Nature Communications, 2022, vol. 13, issue 1, 1-17

Abstract: Abstract Mucosal antibodies maintain gut homeostasis by promoting spatial segregation between host tissues and luminal microbes. Whether and how mucosal antibody responses influence gut health through modulation of microbiota composition is unclear. Here, we use a CD19−/− mouse model of antibody-deficiency to demonstrate that a relationship exists between dysbiosis, defects in bile acid homeostasis, and gluten-sensitive enteropathy of the small intestine. The gluten-sensitive small intestine enteropathy that develops in CD19−/− mice is associated with alterations to luminal bile acid composition in the SI, marked by significant reductions in the abundance of conjugated bile acids. Manipulation of bile acid availability, adoptive transfer of functional B cells, and ablation of bacterial bile salt hydrolase activity all influence the severity of small intestine enteropathy in CD19−/− mice. Collectively, results from our experiments support a model whereby mucosal humoral immune responses limit inflammatory disease of the small bowel by regulating bacterial BA metabolism.

Date: 2022
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DOI: 10.1038/s41467-022-28126-w

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