Alcohol consumption during murine acquired immunodeficiency syndrome accentuates heart pathology due to coxsackievirus

R. Tomás Sepúlveda, Shuguang Jiang, David G. Besselsen, Ronald R Watson

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Alcohol, especially after prolonged and excessive consumption, results in marked alteration of host immunity and increased susceptibility to infection. To determine whether ethanol consumption exacerbates coxsackievirus B3 cardiomyopathy during murine acquired immunodeficiency syndrome (AIDS), female C57BL/6 mice were infected with LP-BM5 retrovirus and administered 40% ethanol both in water and in solid agar-based form. Cardiac histopathology was semi-quantitatively assessed for lesion severity and induced production of splenocyte: interleukin (IL)-2, IL-4, IL-6, tumour necrosis factor-α and interferon-γ were determined. Ethanol consumption during murine retrovirus infection increased coxsackievirus-induced myocarditis in 85% of the animals and also exacerbated the lesion severity. Mice infected with retrovirus and co-infected with coxsackievirus showed significant heart lesions. Retrovirus infection suppressed Th1 responses, causing cytokine dysregulation and immunosuppression, which facilitated coxsackievirus-induced myocarditis. Our data suggest that ethanol consumption heightens the cytokine imbalance to favour a Th2 response by enhancing Th2 and/or by suppressing Th1 function. In conclusion, murine AIDS facilitated severe cardiotoxicity during coxsackievirus infection, while non-retrovirus-infected mice were resistant. These effects were accentuated by ethanol consumption.

Original languageEnglish (US)
Pages (from-to)157-163
Number of pages7
JournalAlcohol and Alcoholism
Volume37
Issue number2
StatePublished - 2002

Fingerprint

Murine Acquired Immunodeficiency Syndrome
Enterovirus
Pathology
Alcohol Drinking
Ethanol
Alcohols
Retroviridae Infections
Myocarditis
Retroviridae
Coxsackievirus Infections
Cytokines
Cardiomyopathies
Inbred C57BL Mouse
Interleukin-4
Immunosuppression
Interferons
Agar
Interleukin-2
Immunity
Interleukin-6

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Toxicology

Cite this

Alcohol consumption during murine acquired immunodeficiency syndrome accentuates heart pathology due to coxsackievirus. / Tomás Sepúlveda, R.; Jiang, Shuguang; Besselsen, David G.; Watson, Ronald R.

In: Alcohol and Alcoholism, Vol. 37, No. 2, 2002, p. 157-163.

Research output: Contribution to journalArticle

Tomás Sepúlveda, R. ; Jiang, Shuguang ; Besselsen, David G. ; Watson, Ronald R. / Alcohol consumption during murine acquired immunodeficiency syndrome accentuates heart pathology due to coxsackievirus. In: Alcohol and Alcoholism. 2002 ; Vol. 37, No. 2. pp. 157-163.
@article{2d53766cebe847d6a4832d8e59eb4003,
title = "Alcohol consumption during murine acquired immunodeficiency syndrome accentuates heart pathology due to coxsackievirus",
abstract = "Alcohol, especially after prolonged and excessive consumption, results in marked alteration of host immunity and increased susceptibility to infection. To determine whether ethanol consumption exacerbates coxsackievirus B3 cardiomyopathy during murine acquired immunodeficiency syndrome (AIDS), female C57BL/6 mice were infected with LP-BM5 retrovirus and administered 40{\%} ethanol both in water and in solid agar-based form. Cardiac histopathology was semi-quantitatively assessed for lesion severity and induced production of splenocyte: interleukin (IL)-2, IL-4, IL-6, tumour necrosis factor-α and interferon-γ were determined. Ethanol consumption during murine retrovirus infection increased coxsackievirus-induced myocarditis in 85{\%} of the animals and also exacerbated the lesion severity. Mice infected with retrovirus and co-infected with coxsackievirus showed significant heart lesions. Retrovirus infection suppressed Th1 responses, causing cytokine dysregulation and immunosuppression, which facilitated coxsackievirus-induced myocarditis. Our data suggest that ethanol consumption heightens the cytokine imbalance to favour a Th2 response by enhancing Th2 and/or by suppressing Th1 function. In conclusion, murine AIDS facilitated severe cardiotoxicity during coxsackievirus infection, while non-retrovirus-infected mice were resistant. These effects were accentuated by ethanol consumption.",
author = "{Tom{\'a}s Sep{\'u}lveda}, R. and Shuguang Jiang and Besselsen, {David G.} and Watson, {Ronald R}",
year = "2002",
language = "English (US)",
volume = "37",
pages = "157--163",
journal = "Alcohol and Alcoholism",
issn = "0735-0414",
publisher = "Oxford University Press",
number = "2",

}

TY - JOUR

T1 - Alcohol consumption during murine acquired immunodeficiency syndrome accentuates heart pathology due to coxsackievirus

AU - Tomás Sepúlveda, R.

AU - Jiang, Shuguang

AU - Besselsen, David G.

AU - Watson, Ronald R

PY - 2002

Y1 - 2002

N2 - Alcohol, especially after prolonged and excessive consumption, results in marked alteration of host immunity and increased susceptibility to infection. To determine whether ethanol consumption exacerbates coxsackievirus B3 cardiomyopathy during murine acquired immunodeficiency syndrome (AIDS), female C57BL/6 mice were infected with LP-BM5 retrovirus and administered 40% ethanol both in water and in solid agar-based form. Cardiac histopathology was semi-quantitatively assessed for lesion severity and induced production of splenocyte: interleukin (IL)-2, IL-4, IL-6, tumour necrosis factor-α and interferon-γ were determined. Ethanol consumption during murine retrovirus infection increased coxsackievirus-induced myocarditis in 85% of the animals and also exacerbated the lesion severity. Mice infected with retrovirus and co-infected with coxsackievirus showed significant heart lesions. Retrovirus infection suppressed Th1 responses, causing cytokine dysregulation and immunosuppression, which facilitated coxsackievirus-induced myocarditis. Our data suggest that ethanol consumption heightens the cytokine imbalance to favour a Th2 response by enhancing Th2 and/or by suppressing Th1 function. In conclusion, murine AIDS facilitated severe cardiotoxicity during coxsackievirus infection, while non-retrovirus-infected mice were resistant. These effects were accentuated by ethanol consumption.

AB - Alcohol, especially after prolonged and excessive consumption, results in marked alteration of host immunity and increased susceptibility to infection. To determine whether ethanol consumption exacerbates coxsackievirus B3 cardiomyopathy during murine acquired immunodeficiency syndrome (AIDS), female C57BL/6 mice were infected with LP-BM5 retrovirus and administered 40% ethanol both in water and in solid agar-based form. Cardiac histopathology was semi-quantitatively assessed for lesion severity and induced production of splenocyte: interleukin (IL)-2, IL-4, IL-6, tumour necrosis factor-α and interferon-γ were determined. Ethanol consumption during murine retrovirus infection increased coxsackievirus-induced myocarditis in 85% of the animals and also exacerbated the lesion severity. Mice infected with retrovirus and co-infected with coxsackievirus showed significant heart lesions. Retrovirus infection suppressed Th1 responses, causing cytokine dysregulation and immunosuppression, which facilitated coxsackievirus-induced myocarditis. Our data suggest that ethanol consumption heightens the cytokine imbalance to favour a Th2 response by enhancing Th2 and/or by suppressing Th1 function. In conclusion, murine AIDS facilitated severe cardiotoxicity during coxsackievirus infection, while non-retrovirus-infected mice were resistant. These effects were accentuated by ethanol consumption.

UR - http://www.scopus.com/inward/record.url?scp=0036130054&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036130054&partnerID=8YFLogxK

M3 - Article

C2 - 11912071

AN - SCOPUS:0036130054

VL - 37

SP - 157

EP - 163

JO - Alcohol and Alcoholism

JF - Alcohol and Alcoholism

SN - 0735-0414

IS - 2

ER -