Alteration of DSS-mediated immune cell redistribution in murine colitis by oral colostral immunoglobulin
1 Division of Gastroenterology, Department of Medicine II, University of Rostock, Rostock 18057, Germany
2 Department of Immunology, Project group “Extracorporal Immunomodulation”, Fraunhofer Institute for Cell Therapy and Immunology, Rostock 18057, Germany
3 Centre for Coordination of Clinical studies, University of Rostock, Rostock, 18057, Germany
4 Department of General, Vascular, Thoracic and Transplantation Surgery, Section of Molecular Oncology and Immunotherapy, University of Rostock, Rostock, 18057, Germany
BMC Immunology 2013, 14:10 doi:10.1186/1471-2172-14-10Published: 20 February 2013
Oral bovine colostrum prophylaxis accelerates the recovery of dextran sulfate sodium (DSS)-induced colitis. In the present study the beneficial effects on acute intestinal inflammation of two major colostral components, secretory immunoglobulin A and lactoferrin, were investigated. Outbred NMRI mice received whole bovine colostrum (BC, 20 mg/kg body weight), colostral bovine lactoferrin (bLf, 150 mg/kg), or secretory immunoglobulin A (sIgA, 1–2 mg/kg body weight) daily by oral gavage, either two weeks before induction of colitis (prophylaxis) or after disease establishment (therapy). Bovine serum albumin (BSA, 150 mg/kg body weight) and immunoglobulin G (IgG, 1 and 2 mg/kg body weight) served as protein controls. Colitis was induced by providing 5% DSS solution ad libitum for seven days.
Compared to BSA, BC therapy improved occult blood, stool consistency, and clinical recovery from colitis but did not prevent initial weight loss. In contrast, administration of bLf did not influence the course of colitis in either the prophylactic or the therapeutic setting. Therapeutic application of sIgA promoted weight gain in the recovery phase of colitis but failed to improve other clinical parameters. Prophylactically-fed sIgA influenced immune cell redistribution, normalized peripheral blood CD11c+CD83+ mature dendritic cells, modulated colonic immune cell infiltration, and altered the numbers of both DSS-induced regulatory γδ TCR+ T cells and CD11b+Gr-1+ myeloid suppressor cells in the lymph nodes and spleens of mice.
These data demonstrated the potential of colostrum in disease recovery and epithelial homeostasis following intestinal injury. Colostral sIgA failed to improve acute disease activity but promoted weight gain and modulated immune cell responses that are involved in the genesis of colitis.