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Clinical and Diagnostic Laboratory Immunology, July 2001, p. 695-701, Vol. 8, No. 4
Nestec SA, Nestlé Research Center, 1000 Lausanne 26, Switzerland
Received 23 December 2000/Returned for modification 7 February
2001/Accepted 15 March 2001
We investigated whether certain strains of lactic acid bacteria
(LAB) could antagonize specific T-helper functions in vitro and thus
have the potential to prevent inflammatory intestinal immunopathologies. All strains tested induced various levels of both
interleukin-12 (IL-12) and IL-10 in murine splenocytes. In particular,
Lactobacillus paracasei (strain NCC2461) induced the highest levels of these cytokines. Since IL-12 and IL-10 have the
potential to induce and suppress Th1 functions, respectively, we
addressed the impact of this bacterium on the outcome of
CD4+ T-cell differentiation. For this purpose, bacteria
were added to mixed lymphocyte cultures where CD4+ T-cells
from naive BALB/c mice were stimulated weekly in the presence of
irradiated allogeneic splenocytes. In these cultures, L. paracasei NCC2461 strongly inhibited the proliferative activity of CD4+ T cells in a dose-dependent fashion. This was
accompanied by a marked decrease of both Th1 and Th2 effector
cytokines, including gamma interferon, IL-4, and IL-5. In contrast,
IL-10 was maintained and transforming growth factor
1071-412X/01/$04.00+0 DOI: 10.1128/CDLI.8.4.695-701.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Induction by a Lactic Acid Bacterium of a
Population of CD4+ T Cells with Low Proliferative Capacity
That Produce Transforming Growth Factor
and
Interleukin-10
(TGF-) was
markedly induced in a dose-dependent manner. The bacteria were not
cytotoxic, because cell viability was not affected after two rounds of
stimulation. Thus, unidentified bacterial components from L. paracasei NCC2461 induced the development of a population of
CD4+ T cells with low proliferative capacity that produced
TGF- and IL-10, reminiscent of previously described subsets of
regulatory cells implicated in oral tolerance and gut homeostasis.
*
Corresponding author. Mailing address: Nestec SA,
Nestlé Research Center, P.O. Box 44, 1000 Lausanne 26, Switzerland. Phone: 41 21 785 89 54. Fax: 41 21 785 89 25. E-mail:
thierry.von-der-weid{at}rdls.nestle.com.
Clinical and Diagnostic Laboratory Immunology, July 2001, p. 695-701, Vol. 8, No. 4
1071-412X/01/$04.00+0 DOI: 10.1128/CDLI.8.4.695-701.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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