1. Loss of PTPN22 abrogates the beneficial effect of cohousing-mediated fecal microbiota transfer in murine colitis
- Author
-
Alina N. Santos, Ali Shawki, Gerhard Rogler, Marlene Schwarzfischer, Gabriel E. Leventhal, Silvia Lang, Christophe Lacroix, Anica Sayoc, Marianne R. Spalinger, Larissa Hering, Katharina Bäbler, David J. Rawlings, Claudia Gottier, Andrew A Chan, Declan F. McCole, Annelies Geirnaert, Xuezhi Dai, and Michael Scharl
- Subjects
0301 basic medicine ,business.industry ,Immunology ,Phosphatase ,Disease ,medicine.disease ,Ulcerative colitis ,PTPN22 ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Genotype ,Immunology and Allergy ,Medicine ,030211 gastroenterology & hepatology ,Colitis ,business ,Cohousing ,Feces - Abstract
Fecal microbiota transfer (FMT) is a very efficient approach for the treatment of severe and recurring C. difficile infections. However, the beneficial effect of FMT in other disorders such as ulcerative colitis (UC) or Crohn's disease remains unclear. Furthermore, it is currently unknown how disease-associated genetic variants in donors or recipients influence the effect of FMT. We found that bacteria-transfer from wild-type (WT) donors via cohousing was efficient in inducing recovery from colitis in WT mice, but not in mice deficient in protein-tyrosine phosphatase non-receptor type 22 (PTPN22), a known risk gene for several chronic inflammatory diseases. Also cohousing of PTPN22-deficient mice with diseased WT mice failed to induce faster recovery. Our data indicate that the genetic background of the donor and the recipient influences the outcome of microbiota transfer, and offers a potential explanation why transfer of fecal microbes from some, but not all donors is efficient in UC patients.
- Published
- 2019
- Full Text
- View/download PDF