Effects of Chronic Ethanol Consumption in Experimental Sepsis

Barros, Flávia Regina Oliveira de; Castro‐Faria‐Neto, Hugo C.; Castro, C.; Nemer, Ala; Rocha, Elisabeth da Silva da Martins; Fonseca, V.

doi:10.1093/alcalc/ags081

Cited by 18 publications

(29 citation statements)

References 31 publications

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“…First, enrolment of subjects by administrative claims data may be less accurate, which is an inherent limitation to all database research. Evidence evaluating the impact of cigarette smoking [29] or alcohol consumption [34,35] on sepsis outcome is still limited and controversial. Nevertheless, it has been reported that obesity may increase the comorbidity of sepsis, but may not influence the mortality [32,33].…”

Section: Discussionmentioning

confidence: 99%

Sleep apnoea patients have higher mortality when confronting sepsis

Huang

Chen

et al. 2013

Eur J Clin Investigation

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Section: Discussionmentioning

confidence: 99%

Sleep apnoea patients have higher mortality when confronting sepsis

Huang

Chen

et al. 2013

Eur J Clin Investigation

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“…We have reported on the same sepsis induction model in male rats exposed to 10% ethanol/water as the only source of liquid for 4 weeks (13). Mortality was directly correlated to ethanol consumption, that is, rats that voluntarily consumed more ethanol (>11 g/kg) died earlier.…”

Section: Discussionmentioning

confidence: 98%

“…No significant differences were found in IL-4 and IL-13. Ethanol significantly decreased the effect of sepsis in the levels of IL-6 and TNF-α (13). …”

Section: Discussionmentioning

confidence: 99%

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Effect of chronic ethanol consumption in female rats subjected to experimental sepsis

Castro

Aguiar-Nemer

Castro‐Faria‐Neto

et al. 2013

Braz J Med Biol Res

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The objective of this research was to evaluate the interference of ethanol consumption by female rats with cytokines involved in the sepsis process and its correlation with mortality, the main outcome of sepsis. Female Wistar rats in estrus phase were evaluated in three experiments. Experiment 1 (n=40) was performed to determine survival rates. Experiment 2 (n=69) was designed for biochemical analysis, measurement of cytokine and estrogen levels before and after sepsis, and experiment 3 (n=10) was performed to evaluate bacterial growth by colony counts of peritoneal fluid. In all experiments, treated animals were exposed to a 10% ethanol/water solution (v/v) as the single drinking source, while untreated animals were given tap water. After 4 weeks, sepsis was induced in the rats by ip injection of feces. In experiment 1, mortality in ethanol-exposed animals was delayed compared with those that drank water (48 h; P=0.0001). Experiment 2 showed increased tumor necrosis factor alpha (TNF-α) and decreased interleukin-6 (IL-6) and macrophage migration inhibitory factor in septic animals exposed to ethanol compared to septic animals not exposed. Sepsis also increased TNF-α and IL-6 levels in both ethanol- and water-exposed groups. Biochemical analysis showed higher creatinine, alanine aminotransferase and aspartate aminotransferase and decreased glucose levels in septic animals that were exposed to ethanol. In experiment 3, septic animals exposed to ethanol showed decreased numbers of colony-forming units than septic animals exposed to water. These results suggest that ethanol consumption delays the mortality of female rats in estrus phase after sepsis induction. Female characteristics, most probably sex hormones, may be involved in cytokine expression.

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“…In a similar rat model of polymicrobial sepsis using intraperitoneal injection of fecal material, Barros et al recently demonstrated a dose-dependent increase in mortality due to sepsis after chronic ethanol ingestion [21]. We hypothesize that this increased mortality is the result of the confluence of multiple immune deficits present in the conditions of both chronic alcohol ingestion and sepsis, but the identities of the key mediators of this effect are not yet known.…”

Section: Introductionmentioning

confidence: 87%

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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Effects of Chronic Ethanol Consumption in Experimental Sepsis

Cited by 18 publications

References 31 publications

Sleep apnoea patients have higher mortality when confronting sepsis

Sleep apnoea patients have higher mortality when confronting sepsis

Effect of chronic ethanol consumption in female rats subjected to experimental sepsis

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

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