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Logo of ccforumBioMed CentralBiomed Central Web Sitesearchsubmit a manuscriptregisterthis articleCritical CareJournal Front Page
Crit Care. 2010; 14(Suppl 1): P13.
Published online 2010 March 1. doi:  10.1186/cc8245
PMCID: PMC2934149

Decreased whole blood TNFα production capacity after acute alcohol exposure and LPS stimulation ex vivo


Acute alcohol exposure is related to increased susceptibility to infections [1]. The purpose of the study was to investigate the effect of acute exposure to different alcohol concentrations in whole blood TNFα production capacity after LPS stimulation ex vivo in healthy men.


Whole blood was taken from healthy volunteers and was placed in tubes containing EDTA and immediately transferred to the lab. Heparinized blood samples diluted 1:10 in RPMI 1640 culture medium (100 μl whole blood added in 900 μl RPMI 1640). Samples were pre-incubated with 0, 5, 12.5, 25, 50, 100 and 200 mM alcohol (EtOH) for 10 minutes at room temperature. After incubation, 500 pg LPS was added in each sample for 4 hours at 37°C. At the end of the process, samples were centrifuged (1,800 rpm, 5 minutes, r.t.). Culture supernatants were collected and stored at -70°C until measurements. TNFα levels were determined in culture supernatant with ELISA [2].


We studied 17 healthy males volunteers aged 36.9 ± 1.6 (X ± SEM). TNFα levels are shown in Figure Figure1.1. There was no TNFα production detected in samples without alcohol in the absence of LPS stimulation (control). TNFα production was significantly decreased at a dose of alcohol of 50 mM after LPS stimulation (P < 0.05) but more apparently at doses of 100 and 200 mM alcohol (P < 0.001) compared with LPS-induced samples.


Alcohol is related to inhibition of TNFα production of whole blood stimulated with LPS ex vivo [3]. This effect occurred shortly after alcohol exposure. Our observation indicates a suppression of proinflammatory response during acute alcoholic intoxication which may be related to increased susceptibility to infections.


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