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Authors: David L. Suskind, Denice Kong, Anne M. Stevens, Ghassan Wahbeh, Denise Christie, Lee-Ann Baxter-Lowe and Marcus O. Muench

David L. Suskind

Corresponding author: David.Suskind@seattlechildrens.org
Department of Pediatrics, Seattle Children’s Hospital and University of Washington; Seattle, Washington, USA

Denice Kong

Department of Immunogenetics, University of San Francisco; San Francisco, California, USA

Anne M. Stevens

Department of Pediatrics, Seattle Children’s Hospital and University of Washington; Seattle, Washington, USA

Ghassan Wahbeh

Department of Pediatrics, Seattle Children’s Hospital and University of Washington; Seattle, Washington, USA

Denise Christie

Department of Pediatrics, Seattle Children’s Hospital and University of Washington; Seattle, Washington, USA

Lee-Ann Baxter-Lowe

Department of Immunogenetics, University of San Francisco; San Francisco, California, USA

Marcus O. Muench

Blood Systems Research Institute and the Department of Laboratory Medicine and the Liver Center, University of California, San Francisco; San Francisco, California, USA

Inflammatory bowel disease (IBD) shares many immunologic and clinical characteristics with graft versus host disease caused by allogeneic T lymphocytes after hematopoietic cell transplantation. Since maternal cells are known to enter the fetal circulation in a high proportion of pregnancies, we hypothesized that maternal engraftment in the fetus results in immune sequelae that can lead to IBD. Method: The presence and extent of maternal microchimerism in tissues and blood samples from patients with Crohn’s, Ulcerative colitis (UC), and control groups were determined using kinetic Polymerase Chain Reaction (kPCR) to detect maternal- and patient-specific HLA types. In addition, fluorescent in situ hybridization (FISH) was employed to detect maternal cells in biopsies from patients with IBD. Results: Using kPCR, maternal microchimerism was observed in 9 of the 16 (56%) patients with IBD and 6 out of 15 of the control group (40%) (P=NS). Five of 10 Crohn’s patients had evidence of maternal microchimerism (50%) (P=NS). Four of 6 UC patients had evidence of maternal microchimerism in gut tissues (67%) (P=NS). There is no correlation between maternal michrochimerism and disease activity, disease location or granulomas in patients with IBD. Using FISH, 5 male Crohn’s and 5 male UC patient’s intestinal biopsies were analyzed for maternal microchimerism. No maternal cells were identified.