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Lactic Acid Bacteria Inducing a Weak Interleukin-12 and Tumor Necrosis Factor Alpha Response in Human Dendritic Cells Inhibit Strongly Stimulating Lactic Acid Bacteria but Act Synergistically with Gram-Negative Bacteria

Lactic Acid Bacteria Inducing a Weak Interleukin-12 and Tumor Necrosis Factor Alpha Response in... The development and maintenance of immune homeostasis indispensably depend on signals from the gut flora. Lactic acid bacteria (LAB), which are gram-positive (G + ) organisms, are plausible significant players and have received much attention. Gram-negative (G – ) commensals, such as members of the family Enterobacteriaceae , may, however, be immunomodulators that are as important as G + organisms but tend to be overlooked. Dendritic cells (DCs) are crucial immune regulators, and therefore, the present study aimed at investigating differences among human gut flora-derived LAB and G – bacteria in their patterns of DC polarization. Human monocyte-derived DCs were exposed to UV-killed bacteria, and cytokine secretion and surface marker expression were analyzed. Profound differences in the DC polarization patterns were found among the strains. While strains of LAB varied greatly in their capacity to induce interleukin-12 (IL-12) and tumor necrosis factor alpha (TNF- ), G – strains were consistently weak IL-12 and TNF- inducers. All strains induced significant amounts of IL-10, but G – bacteria were far more potent IL-10 inducers than LAB. Interestingly, we found that when weakly IL-12- and TNF- -inducing LAB and strong IL-12- and TNF- -inducing LAB were mixed, the weakly IL-12- and TNF- -inducing LAB efficiently inhibited otherwise strong IL-12- and TNF- -inducing LAB, yet when weakly IL-12- and TNF- -inducing LAB were mixed with G – bacteria, they synergistically induced IL-12 and TNF- . Furthermore, strong IL-12- and TNF- -inducing LAB efficiently up-regulated surface markers (CD40, CD83, CD86, and HLA-DR), which were inhibited by weakly IL-12- and TNF- -inducing LAB. All G – bacteria potently up-regulated surface markers; however, these markers were not inhibited by weakly IL-12- and TNF- -inducing LAB. These much divergent DC stimulation patterns among intestinal bacteria, which encompass both antagonistic and synergistic relationships, support the growing evidence that the composition of the gut flora affects immune regulation and that compositional imbalances may be involved in disease etiology. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical and Vaccine Immunology American Society For Microbiology

Lactic Acid Bacteria Inducing a Weak Interleukin-12 and Tumor Necrosis Factor Alpha Response in Human Dendritic Cells Inhibit Strongly Stimulating Lactic Acid Bacteria but Act Synergistically with Gram-Negative Bacteria

Lactic Acid Bacteria Inducing a Weak Interleukin-12 and Tumor Necrosis Factor Alpha Response in Human Dendritic Cells Inhibit Strongly Stimulating Lactic Acid Bacteria but Act Synergistically with Gram-Negative Bacteria

Clinical and Vaccine Immunology , Volume 13 (3): 365 – Mar 1, 2006

Abstract

The development and maintenance of immune homeostasis indispensably depend on signals from the gut flora. Lactic acid bacteria (LAB), which are gram-positive (G + ) organisms, are plausible significant players and have received much attention. Gram-negative (G – ) commensals, such as members of the family Enterobacteriaceae , may, however, be immunomodulators that are as important as G + organisms but tend to be overlooked. Dendritic cells (DCs) are crucial immune regulators, and therefore, the present study aimed at investigating differences among human gut flora-derived LAB and G – bacteria in their patterns of DC polarization. Human monocyte-derived DCs were exposed to UV-killed bacteria, and cytokine secretion and surface marker expression were analyzed. Profound differences in the DC polarization patterns were found among the strains. While strains of LAB varied greatly in their capacity to induce interleukin-12 (IL-12) and tumor necrosis factor alpha (TNF- ), G – strains were consistently weak IL-12 and TNF- inducers. All strains induced significant amounts of IL-10, but G – bacteria were far more potent IL-10 inducers than LAB. Interestingly, we found that when weakly IL-12- and TNF- -inducing LAB and strong IL-12- and TNF- -inducing LAB were mixed, the weakly IL-12- and TNF- -inducing LAB efficiently inhibited otherwise strong IL-12- and TNF- -inducing LAB, yet when weakly IL-12- and TNF- -inducing LAB were mixed with G – bacteria, they synergistically induced IL-12 and TNF- . Furthermore, strong IL-12- and TNF- -inducing LAB efficiently up-regulated surface markers (CD40, CD83, CD86, and HLA-DR), which were inhibited by weakly IL-12- and TNF- -inducing LAB. All G – bacteria potently up-regulated surface markers; however, these markers were not inhibited by weakly IL-12- and TNF- -inducing LAB. These much divergent DC stimulation patterns among intestinal bacteria, which encompass both antagonistic and synergistic relationships, support the growing evidence that the composition of the gut flora affects immune regulation and that compositional imbalances may be involved in disease etiology.

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Publisher
American Society For Microbiology
Copyright
Copyright © 2006 by the American Society For Microbiology.
ISSN
1556-6811
eISSN
1556-6811
DOI
10.1128/CVI.13.3.365-375.2006
Publisher site
See Article on Publisher Site

Abstract

The development and maintenance of immune homeostasis indispensably depend on signals from the gut flora. Lactic acid bacteria (LAB), which are gram-positive (G + ) organisms, are plausible significant players and have received much attention. Gram-negative (G – ) commensals, such as members of the family Enterobacteriaceae , may, however, be immunomodulators that are as important as G + organisms but tend to be overlooked. Dendritic cells (DCs) are crucial immune regulators, and therefore, the present study aimed at investigating differences among human gut flora-derived LAB and G – bacteria in their patterns of DC polarization. Human monocyte-derived DCs were exposed to UV-killed bacteria, and cytokine secretion and surface marker expression were analyzed. Profound differences in the DC polarization patterns were found among the strains. While strains of LAB varied greatly in their capacity to induce interleukin-12 (IL-12) and tumor necrosis factor alpha (TNF- ), G – strains were consistently weak IL-12 and TNF- inducers. All strains induced significant amounts of IL-10, but G – bacteria were far more potent IL-10 inducers than LAB. Interestingly, we found that when weakly IL-12- and TNF- -inducing LAB and strong IL-12- and TNF- -inducing LAB were mixed, the weakly IL-12- and TNF- -inducing LAB efficiently inhibited otherwise strong IL-12- and TNF- -inducing LAB, yet when weakly IL-12- and TNF- -inducing LAB were mixed with G – bacteria, they synergistically induced IL-12 and TNF- . Furthermore, strong IL-12- and TNF- -inducing LAB efficiently up-regulated surface markers (CD40, CD83, CD86, and HLA-DR), which were inhibited by weakly IL-12- and TNF- -inducing LAB. All G – bacteria potently up-regulated surface markers; however, these markers were not inhibited by weakly IL-12- and TNF- -inducing LAB. These much divergent DC stimulation patterns among intestinal bacteria, which encompass both antagonistic and synergistic relationships, support the growing evidence that the composition of the gut flora affects immune regulation and that compositional imbalances may be involved in disease etiology.

Journal

Clinical and Vaccine ImmunologyAmerican Society For Microbiology

Published: Mar 1, 2006

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