Long-term melatonin supplementation does not recover the impairment of natural killer cell activity and lymphocyte proliferation in aging mice

Provinciali, Mauro; Stefano, Giuseppina Di; Bulian, Daniele; Stronati, Stefania; Fabris, Ν.

doi:10.1016/s0024-3205(97)00587-0

Cited by 18 publications

(9 citation statements)

References 14 publications

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“…Melatonin may have direct effects on CD4 but not CD8 cells because of a direct effect on gene regulation via binding the putative nuclear melatonin receptor (347). In vivo treatment with melatonin is reported not to reconstitute age-associated impairment of NK activity or lymphoproliferative responses in mice (348). Consistent with these results in vitro supplementation also failed to reconstitute proliferation or IL 2 production in old rat cells (349).…”

Section: Hormonesmentioning

confidence: 53%

T cells and aging

Pawelec

Remarque²,

Barnett³

et al. 1998

Front Biosci

130

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Deterioration of the immune system with aging ("immunosenescence") is believed to contribute to morbidity and mortality in man due to the greater incidence of infection, as well as possibly autoimmune phenomena and cancer in the aged. Dysregulation of T cell function is thought to play a critical part in these processes. Factors contributing to T cell immunosenescence may include a) stem cell defects, b) thymus involution, c) defects in antigen presenting cells (APC), d) aging of resting immune cells, e) disrupted activation pathways in immune cells, f) replicative senescence of clonally expanding cells. This review aims to consider the current state of knowledge on the scientific basis for and potential clinical relevance of those factors in immunosenescence.

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Section: Hormonesmentioning

confidence: 53%

T cells and aging

Pawelec

Remarque²,

Barnett³

et al. 1998

Front Biosci

130

View full text Add to dashboard Cite

show abstract

“…Melatonin may have direct effects on CD4 but not CD8 cells because of a direct effect on gene regulation via binding the putative nuclear melatonin receptor (555). However, in vivo treatment with melatonin is reported not to reconstitute age-associated impairment of NK activity or lymphoproliferative responses in mice (556). Consistent with these results in vitro supplementation also failed to reconstitute proliferation or IL 2 production in old rat cells (557) or old mouse cells (558).…”

Section: Hormonesmentioning

confidence: 81%

T cells and aging (update February 1999)

Pawelec

1999

Front Biosci

113

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T cell immunosenescence 218effects of dysregulated immune responses in the elderly by supplementation or other approaches may result in an enhancement of their quality of life, and significant reductions in the cost of medical care in old age. FACTORS CONTRIBUTING TO IMMUNO-SENESCENCE HematopoiesisDysregulated hematopoiesis is seen in elderly individuals, raising the possibility that this could contribute to altered immune function in the aged. Hematopoiesis in man may be compromised because of a severely reduced capacity to produce colony stimulating factors (44) and increased production of pro-inflammatory factors such as IL 6 (45), because lower numbers of progenitor cells are present in the BM (46) and because of an age-related decline in proliferative potential of putative haematopoietic stem cells (HSC) (47). In mice, the repopulating potential of murine fetal liver-derived HSC is higher than that of adult BM-derived stem cells (48), suggesting possible aging of the HSC themselves. Normal cells with shorter telomeres possess less remaining replicative capacity than those with longer telomeres (see section 5.2). Accordingly, HSC from adult BM were found to have shorter telomeres than fetal liver-derived or umbilical cord-derived stem cells, consistent with aging of HSC (49). Telomere lengths decreased on culture despite low level expression of telomerase in these cells (50,51), although the rate of basepair loss per population doubling of cells in culture was lower during the first two weeks, when telomerase was upregulated, than in the next two, when it was downregulated (52). The telomerase expressed is therefore functionally active but may not be able to completely maintain telomere length in aging HSC cells. True embryonic stem cells (ESC), on the other hand, which may really be immortal, do retain high levels of telomerase activity (53). On the other hand, ESC from telomerase-knockout mice show gradual telomere shortening over many population doublings (PD) resulting in slowing and eventual cessation of growth (54). Certain animals which do not downregulate telomerase manifest a permanent growth phase and little or no senescence (55,56).

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“…In another study, Provinciali et al. demonstrated that the long‐term melatonin administration in old mice had no effect on the NK cell number. Our data indirectly are in accordance with the statements above.…”

Section: Discussionmentioning

confidence: 98%

Immunoregulatory actions of melatonin and zinc during chronic Trypanosoma cruzi infection

Brazão

Santello

Filipin

et al. 2015

Journal of Pineal Research

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After one century of the discovery of Chagas' disease and the development of an efficient drug with amplitude of actions both in the acute and chronic phase is still a challenge. Alternative immune modulators have been exhaustively used. For that purpose, melatonin and zinc were administered during chronic Trypanosoma cruzi-infected Wistar rats and several endpoints were assessed. Melatonin has a remarkable functional versatility, being associated with important antioxidant, anti-inflammatory, and anti-apoptotic effects. The cross-talk between zinc and the immune system includes its ability to influence the production and signaling of numerous inflammatory cytokines in a variety of cell types. Our study showed that zinc triggered a decrease in the generation of IFN-γ for TCD4(+) cells. Reduced percentage of CD4(+) T cells producing TNF-α was observed in control melatonin or zinc-and-melatonin-treated animals as compared with untreated rats. On the other hand, a significant increase in the percentage of IL-4 from CD4(+) and CD8(+) T lymphocytes producers was observed 60 days after infection, for all zinc-treated animals, whether infected or not. Melatonin and zinc therapies increased the percentages of CD4(+) and CD8(+) T lymphocytes IL-10 producers. CD4(+) CD25(high) Foxp3(+) T cells were also elevated in zinc- and melatonin-treated animals. The modulation of the immune system influenced by these molecules affected cytokine production and the inflammatory process during chronic T. cruzi infection. Elucidation of the interplay between cytokine balance and the pathogenesis of Chagas' disease is extremely relevant not only for the comprehension of the immune mechanisms and clinical forms but, most importantly, also for the implementation of efficient and adequate therapies.

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Long-term melatonin supplementation does not recover the impairment of natural killer cell activity and lymphocyte proliferation in aging mice

Cited by 18 publications

References 14 publications

T cells and aging

T cells and aging

T cells and aging (update February 1999)

Immunoregulatory actions of melatonin and zinc during chronic Trypanosoma cruzi infection

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