Immunosenescence is defined as the state of deregulated immune function that contributes to the increased susceptibility of the elderly to infection and, possibly, to autoimmune diseases and cancer (49,50). When immunosenescence appears, the functional capacity of the immune system of the host gradually declines with age. The most dramatic changes in immune function with age occur within the T cells compartment, the arm of the immune system that protects against pathogens and tumors (51-54). The fact that T lymphocytes are more severely affected than B cells or antigen-presenting cells is mainly due to the involution of the thymus, which is almost complete at the age of 60. The host is then dependent on the T cells of various specificities, which eventually leads to changes in the T cell repertoire. CD45RA + "native" cells are replaced by CD45RA — "memory" cells, and a T cell receptor oligoclonality develops. At the same time, T cells with signal transduction defects accumulate. Age-related T cell alterations lead to a decreased clonal expansion and a reduced efficiency of T cell effectors functions, such as cytotoxicity or B cell functionality. Decreased antibody production and a shortened immunological memory are the consequence. Efficient protection of elderly individuals by suitable vaccination strategies is therefore a matter of great importance (51,55). Perhaps of greater consequence to interpretation of immunosenescence in the elderly is the decline in cellmediated immunity (CMI). This is particularly important with respect to combating infectious disease, but also to tumor surveillance, since anti-tumor effects of the immune system are almost exclusively governed by the cell-mediated component.
Interleukin (IL)-12 is a cytokine produced by mononuclear phagocytes and dendritic cells that serves as a mediator of the innate immune response to intracellular microbes and is a key inducer of cell-mediated immune responses towards microbes (56). IL-12 activates natural killer (NK) cells, promotes interferon (IFN)-g production by NK cells and T cells, enhances cytotoxic activity of NK cells and cytolytic T lymphocytes, and promotes the development of TH1 cells. IL-10 and IL-12 are two cytokines secreted by monocytes/macrophages in response to bacterial products which have largely opposite effects on the immune system. IL-12 activates cytotoxicity and IFN-g secretion by T cells and NK cells, whereas IL-10 inhibits these functions.
Many studies indicate that Gram-positive bacteria and their cell wall components are potent inducers of IL-12 for human monocytes, while the Gram-negative bacteria can promote more IL-10 (57-60). Karlsson and coworkers (61) also reported that Grampositive bacteria B. adolescentis, Enterococcus fecalis, Lactobacillus plantarum, Streptococcus mitis can induce more IL-12 production by mononuclear cells from cord and adult blood compared to the gram-negative bacteria, Bacteroides vulgatus, Escherichia coli, Pseudomonas aeruginosa, Veillonella parvula and Nerisseria sicca. In contrast, more IL-10 was secreted by the stimulation of mononuclear from cord and adults with Gram-negative bacteria instead of gram-positive bacteria.
Furthermore, He and coworkers (62,63) characterized the ability of bifidobacteria to affect the production of macrophage-like derived cytokines with a murine macrophage-like cell line, J774.1 (Fig. 1 and Table 1). B. adolescentis and B. longum, known as adult-type bifidobacteria, induced significantly more pro-inflammatory cytokine secretion, IL-12, and TNF-a by the macrophage-like cells than did infant-type bifidobacteria,
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