Chronic ethanol exposure selectively inhibits the influenza-specific CD8 T cell response during influenza A virus infection

Hemann, Emily A.; McGill, Jodi L.; Waldschmidt, Thomas J.; Legge, Kevin L.

doi:10.1016/j.alcohol.2013.09.017

Cited by 2 publications

(1 citation statement)

References 37 publications

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“…Partlet et al demonstrated selective loss of epidermal and dermal regulatory T cells, specifically due to reduced proliferation and increased apoptosis, as well as decreased expression of JAML and CD69 on dendritic epidermal T cells following ex vivo stimulation and impaired IL-17 responses[11]. Additionally, in a murine model of Influenza A virus (IAV) infection following ethanol ingestion, ethanol was associated with increased mortality, increased viral titers, and decreased IAV-specific CD8 T cells with reduced proliferation, IFN-γ production and degranulation induced target cell lysis[12]. …”

Section: Introductionmentioning

confidence: 99%

Chronic Alcohol Ingestion Delays T Cell Activation and Effector Function in Sepsis

Margoles¹,

Mittal²,

Klingensmith³

et al. 2016

PLoS ONE

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Sepsis is the leading cause of death in intensive care units in the US, and it is known that chronic alcohol use is associated with higher incidence of sepsis, longer ICU stays, and higher mortality from sepsis. Both sepsis and chronic alcohol use are associated with immune deficits such as decreased lymphocyte numbers, impaired innate immunity, delayed-type hypersensitivity reactions, and susceptibility to infections; however, understanding of specific pathways of interaction or synergy between these two states of immune dysregulation is lacking. This study therefore sought to elucidate mechanisms underlying the immune dysregulation observed during sepsis in the setting of chronic alcohol exposure. Using a murine model of chronic ethanol ingestion followed by sepsis induction via cecal ligation and puncture, we determined that while CD4+ and CD8+ T cells isolated from alcohol fed mice eventually expressed the same cellular activation markers (CD44, CD69, and CD43) and effector molecules (IFN-γ, TNF) as their water fed counterparts, there was an overall delay in the acquisition of these phenotypes. This early lag in T cell activation was associated with significantly reduced IL-2 production at a later timepoint in both the CD4+ and CD8+ T cell compartments in alcohol sepsis, as well as with a reduced accumulation of CD8dim activated effectors. Taken together, these data suggest that delayed T cell activation may result in qualitative differences in the immune response to sepsis in the setting of chronic alcohol ingestion.

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Section: Introductionmentioning

confidence: 99%