Ethanol exacerbates T cell dysfunction after thermal injury

Choudhry, Mashkoor A.; Messingham, Kelly A. N.; Namak, Shahla; Colantoni, Alessandra; Fontanilla, Christine V.; Duffner, Lisa A.; Sayeed, M. M.; Kovacs, Elizabeth J.

doi:10.1016/s0741-8329(00)00093-8

Cited by 45 publications

(40 citation statements)

References 30 publications

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“…This finding is likely related to the lower numbers of CD4 ϩ lymphocytes found in the lungs of our LED mice. Alcohol has been reported to have variable effects on IL-2, but in some models, alcohol or its metabolites play a role in the suppression of this cytokine and in diminished lymphocyte proliferation (9,13,39). In our model, the depression of IL-2 levels occurs at day 21, correlating with the time point at which there are significantly fewer CD4 ϩ lymphocytes in the lungs of the LED mice.…”

Section: Discussionmentioning

confidence: 99%

Alcohol Exacerbates Murine Pulmonary Tuberculosis

et al. 2004

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Alcohol consumption has been described as a risk factor for infection with Mycobacterium tuberculosis, but its contribution to tuberculosis has been difficult to isolate from other adverse socioeconomic factors. Our objective was to evaluate the impact of alcohol consumption on pulmonary infection with M. tuberculosis in a murine model. BALB/c mice were maintained on the Lieber-DeCarli liquid ethanol diet or a liquid control diet and infected intratracheally with low-dose M. tuberculosis H37Rv. Lung organism burdens, lung and lung-associated lymph node CD4 ؉ -and CD8 ؉ -lymphocyte numbers and rates of proliferation, and CD4 ؉ -lymphocyte cytokine production levels were compared between the groups. The alcohol-consuming mice had significantly higher lung organism burdens than the control mice, and the CD4 ؉ -and CD8 ؉ -lymphocyte responses to pulmonary infection with M. tuberculosis were blunted in the alcohol group. Lymphocyte proliferation and production of gamma interferon were decreased in the CD4؉ lymphocytes from the alcohol-consuming mice. Additionally, lung granulomas were significantly smaller in the alcohol-consuming mice. In conclusion, murine alcohol consumption is associated with decreased control of pulmonary infection with M. tuberculosis, which is accompanied by alterations in the region-specific CD4؉ -and CD8 ؉ -lymphocyte responses and defective lung granuloma formation.For many years, the medical literature worldwide has suggested an association between alcohol consumption and active tuberculosis in humans (7,10,16,19,23,24,28,44). Screening alcohol-abusing subjects in an urban setting for tuberculous infection revealed rates of active tuberculosis that were 28-fold greater than those of age-matched residents and rates of positive tuberculin tests that were 1.5-fold greater than those of agematched residents of the same locale (19). In another setting, heavy alcohol consumption conferred a twofold-heightened risk for developing active tuberculosis (10). Additionally, a person with active tuberculosis who routinely frequented a neighborhood bar was found to have infected 41 persons who were frequent clients of the bar, one-third of whom developed active tuberculosis (24). Similar reports of increased prevalence of tuberculosis in alcohol-consuming subjects exist outside of the United States. In London, England, regular alcohol use increased the risk of contracting tuberculosis more than twofold (28), and alcohol abuse was found to be a risk factor in the acquisition of multidrug-resistant tuberculosis in Russia (44).However, the bulk of the evidence of an association between alcohol consumption and tuberculosis is circumstantial, and not all studies consistently demonstrate this association (34, 42). Among homeless persons in San Francisco, despite very high rates of tuberculosis, alcohol abuse was not found to be a significant risk factor (34). Regular consumers of alcohol frequently have confounding lifestyle factors, such as other substance (i.e., illicit drugs or tobacco) abuse, low socioeco...

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Section: Discussionmentioning

confidence: 99%

Alcohol Exacerbates Murine Pulmonary Tuberculosis

et al. 2004

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“…Epidemiological studies suggest that moderate alcohol consumption influences cardiovascular risk factors, primarily blood pressure, but also plasma cholesterol and triglyceride levels, platelet function, and fibrinolytic parameters, thereby preventing initiation and progression of atherosclerosis (12,20,21). At the molecular and cellular level, ethanol's actions have been associated with the inhibition of proliferation of many cell types (5,6,11,18), suppressed postprandial vascular smooth muscle cell hypertrophy, a downregulation of PAI-1 expression (15), increased expression of vascular endothelial growth factor and subsequent angiogenesis (16), and stimulation of endothelial NO production and action (35,37). Taken together, most of these mechanisms involved in the beneficial actions of moderate alcohol intake converge in effects that would limit tissue matrix protein production and accumula-tion.…”

Section: Discussionmentioning

confidence: 99%

Moderate alcohol intake has no impact on acute and chronic progressive anti-thy1 glomerulonephritis

Peters

Martini

Woydt

et al. 2003

American Journal of Physiology-Renal Physiology

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Moderate alcohol consumption has shown beneficial effects in experimental and human cardiovascular disease. With the use of rat models of acute and chronic progressive anti-thy1 glomerulonephritis (GN), we tested the hypothesis that moderate alcohol intake is protective in renal fibrotic disease. In acute anti-thy1 GN, untreated nephritic rats showed marked mesangial cell lysis and induced nitric oxide production at day 1 and high proteinuria, glomerular matrix accumulation, and transforming growth factor (TGF)-β1, fibronectin, and plasminogen activator inhibitor (PAI)-1 expression at day 7 after disease induction, respectively. In animals 15 wk after induction of chronic progressive anti-thy1 GN, disease was characterized by significantly reduced renal function, persisting albuminuria as well as increased glomerular and tubulointerstitial matrix expansion, TGF-β1, fibronectin, and PAI-1 protein expression. In both anti-thy1 GN models, an ethanol intake of ∼2 ml per day and animal was achieved, however, disease severity was not significantly altered by moderate alcohol consumption in any of the protocols. In conclusion, moderate alcohol intake does not influence renal matrix protein production and accumulation in acute and chronic progressive anti-thy1 glomerulofibrosis. The study suggests that, in contrast to cardiovascular disorders, moderate alcohol consumption might not provide specific protection in renal fibrotic disease.

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“…Similar changes in immune cells are also noted after acute and chronic alcohol consumption [17][18][19][20][21]. Whereas the clinical evidence showing enhanced morbidity and mortality in burn patients with prior alcohol exposure compared to patients with no alcohol exposure is overwhelming, only a few studies have been carried out to address the underlying mechanism [22][23][24][25][26][27]. These studies have shown that acute alcohol exposure prior to burn injury produced a greater suppression of mitogen-induced splenic-lymphocyte proliferation, serum immunoglobulin levels, and neutrophil chemotaxis [2,[22][23][24][25][26][27].…”

Section: Introductionmentioning

confidence: 99%