The Effect of In Vitro Alcohol Treatment on CD8+ T-cell Senescence

Location

Medical Education Building, LSUHSC-NO

Presentation Date

10-10-2019 10:00 AM

End Date

10-10-2019 12:00 PM

Description

In the United States, rates of heavy drinking among persons living with HIV (PLWH) are higher than those in the general population. Heavy alcohol consumption contributes to accelerated aging of immune cells. As individuals age, a significant proportion of senescent cells accumulate in the body, causing inflammation and damage to the surrounding cells and tissue. Studies have shown that hazardous alcohol consumption accelerates CD8+ T-cell senescence. We have developed a protocol using Activation-Induced Cell Death (AICD) to investigate the phenotype and kinetics of senescent CD8+ T-cells. During AICD, programmed cell death is caused by the interaction of Fas receptors (Fas, CD95) and Fas ligands (FasL, CD95 ligand). We hypothesize that senescent Tcell populations in persons with Alcohol Use Disorder (AUD) will be resistant to AICD. We will analyze the expression of senescence-associated β-galactosidase (SA-β-gal), a biomarker ofcellular senescence, and Annexin V, a marker of apoptosis during AICD, in CD8+ T-cells. We hypothesize that SA-β-gal expression will be highest in CD8+ T-cells stimulated with PHA and exposed to higher concentrations of in vitro alcohol, and the percentage of apoptotic cells will be greater in control cells that were not treated with alcohol.

Comments

Mentor: Dr. Robert W. Siggins II (Department of Physiology & Comprehensive Alcohol Research Center)

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Oct 10th, 10:00 AM Oct 10th, 12:00 PM

The Effect of In Vitro Alcohol Treatment on CD8+ T-cell Senescence

Medical Education Building, LSUHSC-NO

In the United States, rates of heavy drinking among persons living with HIV (PLWH) are higher than those in the general population. Heavy alcohol consumption contributes to accelerated aging of immune cells. As individuals age, a significant proportion of senescent cells accumulate in the body, causing inflammation and damage to the surrounding cells and tissue. Studies have shown that hazardous alcohol consumption accelerates CD8+ T-cell senescence. We have developed a protocol using Activation-Induced Cell Death (AICD) to investigate the phenotype and kinetics of senescent CD8+ T-cells. During AICD, programmed cell death is caused by the interaction of Fas receptors (Fas, CD95) and Fas ligands (FasL, CD95 ligand). We hypothesize that senescent Tcell populations in persons with Alcohol Use Disorder (AUD) will be resistant to AICD. We will analyze the expression of senescence-associated β-galactosidase (SA-β-gal), a biomarker ofcellular senescence, and Annexin V, a marker of apoptosis during AICD, in CD8+ T-cells. We hypothesize that SA-β-gal expression will be highest in CD8+ T-cells stimulated with PHA and exposed to higher concentrations of in vitro alcohol, and the percentage of apoptotic cells will be greater in control cells that were not treated with alcohol.