Long-term caloric restriction ameliorates T cell immunosenescence in mice

Asami, Takuya; Endo, Katsunori; Matsui, Rina; Sawa, Toko; Tanaka, Yuna; Saiki, Takeru; Tanba, Naotaka; Haga, Hadsuki; Tanaka, Sadao

doi:10.1016/j.mad.2022.111710

Cited by 14 publications

(6 citation statements)

References 46 publications

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“…Although many individual undernourished mice lost up to 25% of their body weight, on average, undernourished mice lost 15%±1.5 while control mice gained 3%±0.5 of their original body weight in one week. This undernourishment protocol is similar to dietary restriction models that restrict food access by 50% but is distinct from calorie restriction [20,27].…”

Section: Methodsmentioning

confidence: 99%

Bone marrow by day, lymph nodes by night: Undernutrition imparts a distinct circadian rhythm to T cells in mice

Foster,

Dadzie,

Dunn

et al. 2024

Preprint

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In well-nourished organisms, T cells migrate between the blood and secondary lymphoid organs, conducting surveillance for invading pathogens. T cell surveillance is under circadian control via diurnal fluctuations in corticosterone levels and undernutrition is associated with increased corticosterone. Therefore, we hypothesized that undernutrition disrupts the circadian migratory patterns of T cells. We report that compared to well-nourished controls, undernourished mice demonstrate enhanced T cell relocation to the bone marrow throughout the 24-hour period, but especially during the light phase, and diminished T cell migration to the lymph nodes only during the light phase. Undernutrition-related changes in T cell expression of key migration proteins are also mostly limited to the light phase. For example, undernourished naïve CD4+ T cells exhibited higher levels of CXCR4 and CCR7 as well as reduced levels of S1P1 compared to controls; with all changes, except for CXCR4 expression, being restricted to the light phase. These results suggest that naïve CD4+ T cells in the lymph nodes upregulate CXCR4 during the dark phase, enabling their migration to the bone marrow where they remain for the light phase. Once there, CCR7 is upregulated, presumably sending them back to the lymph node, thereby preserving immunosurveillance during the dark phase. Naïve CD4+ T cell disengagement from S1P1-related egress signals may further contribute to increased retention of cells within each compartment during the appropriate phase. Undernutrition-related increases in T cell residency of the bone marrow likely preserve T cell numbers until nutrition is restored.

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Section: Methodsmentioning

confidence: 99%

Bone marrow by day, lymph nodes by night: Undernutrition imparts a distinct circadian rhythm to T cells in mice

Foster,

Dadzie,

Dunn

et al. 2024

Preprint

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show abstract

“…Moreover, age-related DNA oxidative damage is significantly reduced by caloric restriction, that acts on DNA repair by enhancing pathways such as NER, BER, and double-strand break repair [ 201 ]. A role for caloric restriction in immune regulation and ameliorating immunosenescence has been shown in mice [ 202 ] and in humans [ 203 ], with beneficial effects in stem cell function [ 204 , 205 ].…”

Section: Impact Of Rejuvenating Strategies In Brain Functionmentioning

confidence: 99%

Ageing in the brain: mechanisms and rejuvenating strategies

Gaspar-Silva

Trigo

Magalhaes

2023

Cell. Mol. Life Sci.

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Ageing is characterized by the progressive loss of cellular homeostasis, leading to an overall decline of the organism’s fitness. In the brain, ageing is highly associated with cognitive decline and neurodegenerative diseases. With the rise in life expectancy, characterizing the brain ageing process becomes fundamental for developing therapeutic interventions against the increased incidence of age-related neurodegenerative diseases and to aim for an increase in human life span and, more importantly, health span. In this review, we start by introducing the molecular/cellular hallmarks associated with brain ageing and their impact on brain cell populations. Subsequently, we assess emerging evidence on how systemic ageing translates into brain ageing. Finally, we revisit the mainstream and the novel rejuvenating strategies, discussing the most successful ones in delaying brain ageing and related diseases.

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“…For example, age and caloric intake are critical factors for determining immune response, including one generated in the BM. 58,[75][76][77][78] The increase in BM adiposity decreases all progenitor classes belonging to CD45 + hematopoietic cells, including multipotent progenitor (MPP) cells, common lymphoid progenitors (CLPs), common myeloid progenitors (CMPs), and granulocyte-macrophage progenitor (GMP) cells under homeostasis (Figure 2), independent of age and weight. 79 Furthermore, the increased BM adiposity in leptindeficient obese mice decreases the number of CLPs and the primitive colony forming units (CFU, used as a model for early myelopoiesis) or early hematopoietic progenitors (have CD34 ++ CD38 À immunophenotype) 79 (Figure 2).…”

Section: Obesity Impacts Bm Adiposity Lymphopoiesis and Myelopoiesismentioning

confidence: 99%

Obesity, bone marrow adiposity, and leukemia: Time to act

Kumar,

Stewart

2023

Obesity Reviews

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SummaryObesity has taken the face of a pandemic with less direct concern among the general population and scientific community. However, obesity is considered a low‐grade systemic inflammation that impacts multiple organs. Chronic inflammation is also associated with different solid and blood cancers. In addition, emerging evidence demonstrates that individuals with obesity are at higher risk of developing blood cancers and have poorer clinical outcomes than individuals in a normal weight range. The bone marrow is critical for hematopoiesis, lymphopoiesis, and myelopoiesis. Therefore, it is vital to understand the mechanisms by which obesity‐associated changes in BM adiposity impact leukemia development. BM adipocytes are critical to maintain homeostasis via different means, including immune regulation. However, obesity increases BM adiposity and creates a pro‐inflammatory environment to upregulate clonal hematopoiesis and a leukemia‐supportive environment. Obesity further alters lymphopoiesis and myelopoiesis via different mechanisms, which dysregulate myeloid and lymphoid immune cell functions mentioned in the text under different sequentially discussed sections. The altered immune cell function during obesity alters hematological malignancies and leukemia susceptibility. Therefore, obesity‐induced altered BM adiposity, immune cell generation, and function impact an individual's predisposition and severity of leukemia, which should be considered a critical factor in leukemia patients.

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Long-term caloric restriction ameliorates T cell immunosenescence in mice

Cited by 14 publications

References 46 publications

Bone marrow by day, lymph nodes by night: Undernutrition imparts a distinct circadian rhythm to T cells in mice

Bone marrow by day, lymph nodes by night: Undernutrition imparts a distinct circadian rhythm to T cells in mice

Ageing in the brain: mechanisms and rejuvenating strategies

Obesity, bone marrow adiposity, and leukemia: Time to act

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