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Probiotic modulation of dendritic cell function is influenced by ageing

You, J., Dong, H., Elizabeth, M., Stella, K. and Yaqoob, P. (2014) Probiotic modulation of dendritic cell function is influenced by ageing. Immunobiology, 219 (2). pp. 138-148. ISSN 0171-2985

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To link to this item DOI: 10.1016/j.imbio.2013.08.012

Abstract/Summary

Dendritic cells (DCs) are critical for the generation of T-cell responses. DC function may be modulated by probiotics, which confer health benefits in immunocompromised individuals, such as the elderly. This study investigated the effects of four probiotics, Bifidobacterium longum bv. infantis CCUG 52486, B. longum SP 07/3, L. rhamnosus GG (L.GG) and L. casei Shirota (LcS) on DC function in an allogeneic mixed leucocyte reaction (MLR) model, using DCs and T-cells from young and older donors in different combinations. All four probiotics enhanced expression of CD40, CD80 and CCR7 on both young and older DCs, but enhanced cytokine production (TGF-β, TNF-α) by old DCs only. LcS induced IL-12 and IFNγ production by DC to a greater degree than other strains, while Bifidobacterium longum bv. infantis CCUG 52486 favoured IL-10 production. Stimulation of young T cells in an allogeneic MLR with DC was enhanced by probiotic pretreatment of old DCs, which demonstrated greater activation (CD25) than untreated controls. However, pretreatment of young or old DCs with LPS or probiotics failed to enhance the proliferation of T-cells derived from older donors. In conclusion, this study demonstrates that ageing increases the responsiveness of DCs to probiotics, but this is not sufficient to overcome the impact of immunosenescence in the MLR.

Item Type:Article
Refereed:Yes
Divisions:Interdisciplinary centres and themes > Centre for Food Security
Life Sciences > School of Chemistry, Food and Pharmacy > Department of Food and Nutritional Sciences > Human Nutrition Research Group
ID Code:35633
Uncontrolled Keywords:Ageing; Allogeneic mixed leucocyte reaction; Cytokine; Dendritic cells; Probiotics
Publisher:Elsevier

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