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Mediators of Inflammation
Volume 2013, Article ID 573576, 12 pages
http://dx.doi.org/10.1155/2013/573576
Research Article

Dysregulated Circulating Dendritic Cell Function in Ulcerative Colitis Is Partially Restored by Probiotic Strain Lactobacillus casei Shirota

1Antigen Presentation Research Group, Imperial College London, Northwick Park and St. Mark’s Campus, Level 7W St. Mark’s Hospital, Watford Road, Harrow HA1 3UJ, UK
2Department of Food and Nutritional Sciences, University of Reading, Reading, UK
3Northwick Park Institute for Medical Research, Harrow, UK
4St. Mark’s Hospital, North West London Hospitals NHS Trust, Harrow, UK
5Yakult UK Ltd., West End Road, South Ruislip, UK

Received 4 February 2013; Revised 29 May 2013; Accepted 30 May 2013

Academic Editor: Eduardo Arranz

Copyright © 2013 Elizabeth R. Mann et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. Dendritic cells regulate immune responses to microbial products and play a key role in ulcerative colitis (UC) pathology. We determined the immunomodulatory effects of probiotic strain Lactobacillus casei Shirota (LcS) on human DC from healthy controls and active UC patients. Methods. Human blood DC from healthy controls (control-DC) and UC patients (UC-DC) were conditioned with heat-killed LcS and used to stimulate allogeneic T cells in a 5-day mixed leucocyte reaction. Results. UC-DC displayed a reduced stimulatory capacity for T cells ( ) and enhanced expression of skin-homing markers CLA and CCR4 on stimulated T cells ( ) that were negative for gut-homing marker 7. LcS treatment restored the stimulatory capacity of UC-DC, reflecting that of control-DC. LcS treatment conditioned control-DC to induce CLA on T cells in conjunction with 7, generating a multihoming profile, but had no effects on UC-DC. Finally, LcS treatment enhanced DC ability to induce TGF production by T cells in controls but not UC patients. Conclusions. We demonstrate a systemic, dysregulated DC function in UC that may account for the propensity of UC patients to develop cutaneous manifestations. LcS has multifunctional immunoregulatory activities depending on the inflammatory state; therapeutic effects reported in UC may be due to promotion of homeostasis.