Functional Analysis of T Lymphocyte Subsets in Chronic Experimental Alcoholism in Rats

Bagasra, Omar; Howeedy, A; Kajdacsy-Balla, André

doi:10.1111/j.1749-6632.1987.tb48688.x

Cited by 18 publications

(27 citation statements)

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“…Ethanol impairs T-and B-lymphocyte function and alters immunoglobulin production and secretion of proinflammatory cytokines such as tumor necrosis factor-␣, interleukin-1␤, and interleukin-6. [45][46][47][48] Our findings that chronic alcohol exposure decreased levels of human IFN-␥-producing CD8 ϩ T lymphocytes in blood could be one mechanism for augmented viremia in ethanol-fed HIVE mice. One possible mechanism of inefficient elimination of HIV-1-infected MDMs may be associated with decreased migration of effector CD8 ϩ lymphocytes into the brain.…”

Section: Discussionmentioning

confidence: 99%

Alcohol Abuse Enhances Neuroinflammation and Impairs Immune Responses in an Animal Model of Human Immunodeficiency Virus-1 Encephalitis

Potula

Haorah

Knipe

et al. 2006

The American Journal of Pathology

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Section: Discussionmentioning

confidence: 99%

Alcohol Abuse Enhances Neuroinflammation and Impairs Immune Responses in an Animal Model of Human Immunodeficiency Virus-1 Encephalitis

Potula

Haorah

Knipe

et al. 2006

The American Journal of Pathology

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“…35,36 Chronic alcohol abuse has been shown in experimental models to induce a transient T suppressor cell dysfunction. 37,38 It would indirectly release the regulatory control over the immune system and, therefore, act as a stimulant for CD4 lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

Effect of alcohol consumption on serum hepatitis C virus RNA and histological lesions in chronic hepatitis C

et al. 1998

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The role of alcohol intake in the occurrence of severe liver disease in chronic hepatitis C virus (HCV) carriers is still debated. A cross-sectional study has been conducted in 233 chronic hepatitis C virus carriers. Weekly self-reported alcohol consumption (SRAC) was evaluated, serum HCV RNA levels were measured by a branched DNA technique (Quantiplex 2.0) and HCV genotypes were determined. A liver biopsy was performed simultaneously and liver lesions were graded with the Knodell histological activity index. Data were examined by uni-and multivariate analyses. Alcohol consumption was relatively low (F 140 g/per week in 193/233 patients [80%]). We found a highly significant correlation between SRAC and serum HCV RNA levels (r ‫؍‬ .26, P ‫؍‬ .001). Fibrosis was significantly correlated with age and alcohol consumption. These results suggest that in HCV carriers, alcohol consumption, even with low alcohol intake, increases viremia and hepatic fibrosis. Chronic HCV carriers should be advised to avoid regular alcohol intake. (HEPATOLOGY 1998;27:1717-1722.)The natural course of HCV infection is probably modulated by several cofactors. The role of virus-related factors, namely genotypes and viremia has been extensively studied 1-7 but still remains debated. 8 Up to now, immunological factors were underestimated but several arguments implicate the role of immune response in the course of the disease. Environmental factors and particularly alcohol intake are probably major factors, 9-10 and the increased severity of the disease and the faster occurrence of cirrhosis in patients with HCV infection and heavy alcohol intake has been suggested in several studies. [11][12] Moreover relations between alcohol and the immune response have been suggested with other viral infections. 13 The aim of the present study is to describe the effect of moderate alcohol intake on serum HCV RNA levels and histological liver lesions in patients with chronic HCV infection.

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“…Several studies have shown that there is a potential interaction between alcohol and several other drugs of abuse and HIV-1 infection (26,30,51). Chronic consumption of alcohol can alter various functions of the immune system, including both humoral and cell-mediated processes (8,38). It has been suggested that exposure to EtOH may both increase susceptibility to HIV infection and stimulate HIV replication in previously infected cells and also alter cytokines that increase HIV-1 replication from a quiescent state (7,9,22,(71)(72)(73).…”

Section: Coculturing Of Infected T Cells With Neurons or Neurons Expomentioning

confidence: 99%

Cholesterol-Depleting Statin Drugs Protect Postmitotically Differentiated Human Neurons against Ethanol- and Human Immunodeficiency Virus Type 1-Induced Oxidative Stress In Vitro

Acheampong

Parveen

Mengistu

et al. 2007

J Virol

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The AIDS-related dementia characterized by cognitive dysfunction, motor neuron disease, coordination abnormalities, and other neurological signs and symptoms develops in many human immunodeficiency virus type 1 (HIV-1)-infected individuals (17, 58). The molecular mechanisms involved in these HIV-1-associated dysfunctions of the central nervous system (CNS) remain incompletely explained and controversial (42,45). Studies have demonstrated that although the major reservoirs for productive infection within the CNS of HIV-1-infected individuals are microglia and monocytes/macrophages, infection of other CNSbased cell types, such as microvascular endothelial cells and neurons, also appears to occur (44,57,92). The role of lymphocytes in AIDS dementia has also been described previously (59,67,68). Of note, viral replication in cerebrospinal fluid is considered to be a marker for the severity of AIDS-related neurodegeneration (16,20). The CNS tissues are protected from the periphery by a structure known as blood-brain barrier (BBB), which limits the passage of solutes as well as infections into the brain (10). The tight junctions of brain microvascular endothelial cells strengthen the functional impermeability of BBB. Under certain pathological conditions, the BBB becomes compromised, providing access for infections/infected cells into the brain (64). The passage of HIV-1 entry into the brains of AIDS patients in vivo is not quite clear and is supposed to involve both free viruses and virally infected cells (4,89,91).HIV-1-infected individuals are under chronic oxidative stress, and antioxidants have proved to ameliorate infectionassociated oxidative stress. (81, 84). Oxidative stress involves

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Functional Analysis of T Lymphocyte Subsets in Chronic Experimental Alcoholism in Rats

Cited by 18 publications

References 0 publications

Alcohol Abuse Enhances Neuroinflammation and Impairs Immune Responses in an Animal Model of Human Immunodeficiency Virus-1 Encephalitis

Alcohol Abuse Enhances Neuroinflammation and Impairs Immune Responses in an Animal Model of Human Immunodeficiency Virus-1 Encephalitis

Effect of alcohol consumption on serum hepatitis C virus RNA and histological lesions in chronic hepatitis C

Cholesterol-Depleting Statin Drugs Protect Postmitotically Differentiated Human Neurons against Ethanol- and Human Immunodeficiency Virus Type 1-Induced Oxidative Stress In Vitro

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