Ethanol Blocks Leukocyte Recruitment and Endothelial Cell Activation In Vivo and In Vitro

Saeed, Rubina; Varma, Santosh K.; Peng, Tina; Tracey, Kevin J.; Sherry, Barbara; Metz, Christine N.

doi:10.4049/jimmunol.173.10.6376

Cited by 73 publications

(66 citation statements)

References 71 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Chronic ethanol consumption is linked to a number of abnormalities of the immune system, including lymphopenia, and downregulation of certain costimulatory molecules on the T cell surface (20), as well as to decreased interaction between leukocytes and endothelial cells (21). Chronic ethanol abuse will typically lead to severe medical consequences, but the potential of beneficial consequences of moderate alcohol intake have been discussed for decades, e.g., with respect to the epidemiology of cardiovascular diseases (22)(23)(24)(25).…”

Section: Discussionmentioning

confidence: 99%

Ethanol prevents development of destructive arthritis

Jonsson

Verdrengh

Brisslert

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Environmental factors are thought to play a major role in the development of rheumatoid arthritis. Because the use of ethanol is widespread, we assessed the role of ethanol intake on the propensity to develop chronic arthritis. Collagen type II-immunized mice were given water or water containing 10% (vol/vol) ethanol or its metabolite acetaldehyde. Their development of arthritis was assessed, as well as the impact of ethanol on leukocyte migration and activation of intracellular transcription factors. Mice exposed daily to this dose of ethanol did not display any liver toxicity, and the development of erosive arthritis was almost totally abrogated. In contrast, the antibody-mediated effector phase of collageninduced arthritis was not influenced by ethanol exposure. Also, the major ethanol metabolite, acetaldehyde, prevented the development of arthritis. This antiinflammatory and antidestructive property of ethanol was mediated by (i) down-regulation of leukocyte migration and (ii) up-regulation of testosterone secretion, with the latter leading to decreased NF-B activation. We conclude that low but persistent ethanol consumption delays the onset and halts the progression of collagen-induced arthritis by interaction with innate immune responsiveness.inflammation ͉ cytokines ͉ sex hormones ͉ antibodies ͉ immunity E xcessive alcohol consumption depresses the immune system and increases the propensity to severe bacterial infections, including pneumonia (1), tuberculosis (2), and bacterial peritonitis (3), and to viral infections (4-6). However, some epidemiological studies have suggested that light to moderate ethanol consumption has protective effects against several diseases including chronic heart diseases (7, 8) and ischemic stroke (9).Ethanol consumption has also been implicated in the pathogenesis of systemic lupus erythematosus (SLE), a complex autoimmune disease in the development of which environmental and genetic factors interact. Indeed, some investigators have found that exposure to ethanol is associated with a lower risk for developing SLE (10, 11), whereas others did not observe any effect of alcohol consumption on the incidence of SLE (12, 13). The association between ethanol and rheumatoid arthritis (RA) has been discussed in some studies, but definite conclusions could not be drawn (14-16). Studies so far have been of an epidemiological nature and therefore have not provided any hints about the biological mechanisms of environmental stimuli in the development of autoimmune disease. Our aim here was to assess whether low but persistent consumption of ethanol in quantities nontoxic to liver might affect the incidence and disease manifestation of collagen type II (CII)-induced arthritis (CIA), an established model of human RA. Our results suggest that ethanol intake delays the onset and halts the progression of destructive arthritis. Results Effect of Ethanol Consumption on Development of CIA.To assess whether ethanol drinking has any impact on the development of CIA, CII-immunized mice were provided w...

show abstract

Section: Discussionmentioning

confidence: 99%

Ethanol prevents development of destructive arthritis

Jonsson

Verdrengh

Brisslert

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…Extensive literature has documented the capacity of ethanol to modulate the immune system directly or indirectly by interfering with the function of T lymphocytes, monocytes, macrophages, dendritic cells, neutrophils, and endothelial cells (3)(4)(5)(6)(7)(8). Recent results have provided evidence that two other short chain alcohols also possess a discernible immunomodulatory footprint.…”

mentioning

confidence: 97%

The Size of the Unbranched Aliphatic Chain Determines the Immunomodulatory Potency of Short and Long Chain n-Alkanols

Carignan

Désy

Ghani

et al. 2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Aliphatic n-alkanols have multiple biological effects not yet completely characterized. Results: n-Alkanols are immunomodulators that act downstream of the cell membrane by dysregulating the activation of the NFAT and NF-B transcription factors. Conclusion: There is a correlation between the immunomodulatory capacity of the homologous series of n-alkanols and the size of the aliphatic chain/hydrophobicity. Significance: This work contributes to the understanding of the biological activity of ubiquitous n-alkanols.

show abstract

“…It is possible that alcohol is proapoptotic and acts like aspirin (Chang et al, 2004) by inhibiting the transcription nuclear factorkB (Guizzetti et al, 2003;Saeed et al, 2004). Nuclear factor-kB initiates transcription of antiapoptotic genes such as bcl-2 and has been found to be constitutively activated in the Hodgkin and Reed -Sternberg (HRS) cells (Kuppers and Hansmann, 2005) blocking in this manner the apoptotic pathway.…”

mentioning

confidence: 99%

Tobacco smoking, alcohol drinking and Hodgkin's lymphoma: a European multi-centre case–control study (EPILYMPH)

et al. 2006

View full text Add to dashboard Cite

We analysed the effects of tobacco and alcohol in the aetiology of Hodgkin's lymphoma (HL), based on 340 cases and 2465 controls enrolled in Spain, France, Italy, Germany, Ireland and Czech Republic, between 1998 and2004. Current smokers showed a significantly increased odds ratio (OR) of HL of 1.39 (95% confidence interval (CI) ¼ 1.04 -1.87). Analyses were also conducted separately for subjects younger than 35 years (179 cases) and for older subjects (161 cases). For subjects below age 35, no association was observed between tobacco and HL, whereas for older subjects, ever-smokers experienced a doubled risk of HL as compared to never smokers and the OR of HL for current smoking was 2.35 (95% CI ¼ 1.52 -3.61), with suggestion of a doseresponse relationship. A protective effect of alcohol was observed in both age groups. The OR for ever-regular drinking was 0.58 (95% CI ¼ 0.38 -0.89) for younger subjects and 0.50 (95% CI ¼ 0.34 -0.74) for older subjects. There was no evidence of interaction between tobacco and alcohol. Our results are consistent with previous studies, suggesting a protective effect of alcohol on HL. An effect of tobacco was suggested for HL occurring in middle and late age, although this finding might have occurred by chance.

show abstract

Ethanol Blocks Leukocyte Recruitment and Endothelial Cell Activation In Vivo and In Vitro

Cited by 73 publications

References 71 publications

Ethanol prevents development of destructive arthritis

Ethanol prevents development of destructive arthritis

The Size of the Unbranched Aliphatic Chain Determines the Immunomodulatory Potency of Short and Long Chain n-Alkanols

Tobacco smoking, alcohol drinking and Hodgkin's lymphoma: a European multi-centre case–control study (EPILYMPH)

Contact Info

Product

Resources

About