The effect of aging on liver inflammation: Nothobranchius furzeri as a promising model
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- Aging is defined as the natural and progressive accumulation of physiological changes over time, which lead to diseases and inevitably to death. With current improvements in the health care system, the average human lifespan has greatly increased. However, advanced age is correlated with the onset of several diseases such as metabolic syndrome, cancers, cardiovascular diseases, and neurodegenerative diseases. Aging has been defined with twelve hallmarks, one recently added hallmark is chronic inflammation. Although inflammation is a natural defense mechanism, if it is not resolved it can lead to chronic inflammation that can negatively impact immune cells. A new term has emerged to describe this chronic age dependent inflammation: inflammaging, which has been defined as a dysregulation of the inflammation response and is characterized by an increased production of pro-inflammatory cytokines accompanied with a decreased production of anti-inflammatory cytokines. For example, key pro-inflammatory cytokines involved in inflammation include TNF- α, IL-8, IL-1 β, IL-6 and TLR2, whereas key anti-inflammatory cytokines include IL-10, APOA-1 and SIRT-1. Nothobranchius furzeri are a relatively new animal model to examine the underlying molecular and cellular mechanisms of aging. Results have begun to emerge that markers of inflammaging have been detected in the optic system of N. furzeri. We wish to further explore whether the expression of the above cytokines is impacted by advanced age in other tissues of N. furzeri. Previously, we found little evidence that age altered the expression of these genes in whole brain tissue homogenates. The aim of this present thesis is to address whether the same is true or not for liver tissue, another tissue that is susceptible to age-induced inflammation. Real time-qPCR experiments were conducted on eight genes associated with inflammation (IL-10, TLR2, APOA-1, IL-8, TNF-α, IL1-β, SIRT-1 and IL-6) across four ages (6, 14, 20 and 26 weeks). Out of the eight genes, we were able to measure gene expression across aging for four of them: two anti-inflammatory molecules IL-10 and APOA-1, as well as two pro-inflammatory molecules TLR2 and IL-8. The expression of IL-10 was significantly up-regulated at 14, 20 and 26 weeks of age compared to 6 weeks. In contrast, we did not detect any differences in gene expression of IL-8, TLR2 and APOA-1 across the four ages. Gene expression was also not impacted by biological sex.
Citations
Deflandre, K. (2024). The effect of aging on liver inflammation: Nothobranchius furzeri as a promising model. https://dial-mem.test.bib.ucl.ac.be/handle/2078.2/37132