Antigen-presenting cells exposed to Lactobacillus acidophilus NCFM, Bifidobacterium bifidum BI-98, and BI-504 reduce regulatory T cell activity.
BACKGROUND
The effect in vitro of six different probiotic strains including Lactobacillus acidophilus NCFM, Lactobacillus salivarius Ls-33, Lactobacillus paracasei subsp. paracasei YS8866441, Lactobacillus plantarum Lp-115, Bifidobacterium bifidum BI-504 and BI-98 was studied on splenic enteroantigen-presenting cells (APC) and CD4(+)CD25(+) T-regulatory cells (Tregs) in splenocyte-T cell proliferation assays.


METHODS
Splenocytes exposed to enteroantigen +/- probiotics were used to stimulate cultured CD4(+)CD25(-) T cells to which titrated numbers of Tregs were added. Cytokine assays were performed by use of neutralizing antibodies and ELISA.


RESULTS
Exposure of APCs to enteroantigens and the series of probiotic strains mentioned above did not influence the stimulatory capacity of APCs on proliferative enteroantigen-specific T cells. However, exposure to B. bifidum BI-98, BI-504 and L. acidophilus NCFM consistently reduced the suppressive activity of Tregs. The suppressive activity was analyzed using fractionated components of the probiotics, and showed that a component of the cell wall is responsible for the decreased Treg activity in the system. The probiotic-induced suppression of Treg function is not mediated by changes in APC-secretion of the inflammatory cytokines IL-6 or IL-1b.


CONCLUSIONS
We conclude that certain probiotic strains can modify APCs to cause reduced Treg activity. This effect apparently depends on a direct APC-to-Treg cell contact. The APC-mediated suppressive effect on Treg function of certain probiotic strains may constrain the anti-inflammatory activity, which is often desired from probiotic therapy. This unexpected function of certain probiotic strains should be taken into consideration when designing adjuvant therapies with these bacteria, or when probiotic strains are selected for improvement of gut-associated inflammation like IBD.
Schmidt
Esben Gjerløff Wedebye
EG
Department of International Health, Immunology and Microbiology, University of Copenhagen, Panum Institute, Denmark.
Claesson
Mogens Helweg
MH
Jensen
Simon Skjøde
SS
Ravn
Peter
P
Kristensen
Nanna Ny
NN
D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology / Q000382:microbiology; D000942:Antigens, Bacterial / Q000276:immunology; D001644:Bifidobacterium / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000382:microbiology; D002455:Cell Division / Q000276:immunology; D002478:Cells, Cultured; D005243:Feces / Q000382:microbiology; D005260:Female; D015212:Inflammatory Bowel Diseases / Q000276:immunology* / Q000628:therapy*; D016753:Interleukin-10 / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D019344:Lactic Acid / Q000378:metabolism; D007779:Lactobacillus acidophilus / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D019936:Probiotics / Q000494:pharmacology*; D013154:Spleen / Q000166:cytology / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*
D000942:Antigens, Bacterial; D053583:Interleukin-1beta; D015850:Interleukin-6; D016753:Interleukin-10; D019344:Lactic Acid