Delayed hypersensitivity in alcoholic cirrhosis

Straus, B; Berenyi, Magdalena R.; Huang, Ji-Ming; Straus, Eugene

doi:10.1007/bf02235541

Cited by 74 publications

(9 citation statements)

References 13 publications

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“…The majority of patients with alcoholic liver cirrhosis have a critically impaired immune response which frequently represents a serious clinical problem [1][2][3][4][5][6][7][8][9]. The underlying mechanisms responsible for this defect are unkown.…”

Section: Discussionmentioning

confidence: 99%

“…Patients with liver cirrhosis have an impaired immune response. They are frequently anergic in intracutaneous tests to a set of diverse antigens, have an increased incidence of infection, and often fail to respond to vaccinations such as hepatitis B virus (HBV) vaccine [1][2][3][4][5][6][7][8][9]. A coordinate interaction of different cell types (T cells, B cells, antigen-presenting cells (APC)) with their respective cell surface receptors is required to mount an immune response against a given antigen such as a vaccine [10].…”

Section: Introductionmentioning

confidence: 99%

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Analysis of T cell activation pathways in patients with liver cirrhosis, impaired delayed hypersensitivity and other T cell-dependent functions

Jung²,

Zachoval

et al. 1997

Clinical and Experimental Immunology

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SUMMARYPatients with cirrhosis of the liver frequently demonstrate anergy in intracutaneous tests and fail to respond to vaccination, suggesting impaired delayed hypersensitivity and other T cell-dependent functions in vivo. T cell activation through the coordinated interaction of different cells of the immune system (B cell, antigen-presenting cells (APC)) is an important step in the induction of cellular and humoral immune responses. Impaired T cell-dependent functions in patients with liver cirrhosis may thus be explained by defective T cell activation. We prospectively investigated T cell activation pathways in 12 patients (nine males, three females) with alcoholic liver cirrhosis (seven Child Pugh stage A and B (CP A + B), five Child Pugh stage C (CP C)) and five healthy controls and compared the in vitro results of T cell activation with data obtained in vivo, e.g. intracutaneous tests and vaccination against hepatitis B surface antigen (HBs-Ag). Five out of eight patients who completed vaccination against hepatitis B virus infection were non-responders; one of the three responders had a non-protective antiHBs titre. Moreover, three of five patients with alcoholic liver cirrhosis CP A + B, and two out of three with CP C were anergic in intracutaneous tests to a set of diverse antigens. All parameters of T cell activation were normal, including proliferation mediated by CD2, CD3-T cell receptor (TCR) complex, and CD28; acquisition of responsiveness to exogenous IL-2 and IL-4; activation of proteinkinase C (PKC) by phorbol ester and calcium influx by addition of ionomycin. The ability of monocytes to deliver costimulatory signals was preserved in patients with alcoholic cirrhosis. In addition, serum of patients with alcoholic liver disease did not inhibit T cell proliferation. We conclude that, although in patients with alcoholic liver cirrhosis T cell-dependent functions are impaired in vivo, T cell activation pathways are not responsible for the observed immune defect.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Analysis of T cell activation pathways in patients with liver cirrhosis, impaired delayed hypersensitivity and other T cell-dependent functions

Jung²,

Zachoval

et al. 1997

Clinical and Experimental Immunology

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“…A positive skin response was only shown in 32% of the patients with alcoholic disease (Straus et al, 1971).…”

Section: Ethanol and Cellular Immunitymentioning

confidence: 95%

Influence of alcohol consumption on immunological status: a review

et al. 2002

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The aim of this review is to present and discuss the effect of different levels of alcohol consumption on the immune system. Not only the amount consumed but also the type of alcoholic beverage have to be taken into account in order to determine the consequences on activity, number, distribution, balance, interaction and response of immunocompetent cells. The association between alcohol exposure and the risk of developing an alcohol-related disease is multifactorial. In fact, age, gender, smoking habits, dietary intake and exercise are involved among other factors. The evaluation of the host cellular and humoral immune responses has shown that alcohol may induce some benefits when consumption is moderate. Moreover, those alcoholic beverages that contain antioxidants, such as red wine, could be protectors against immune cell damage. According to the literature consulted, the daily consumption of 10 -12 g and 20 -24 g of alcohol for women and men, respectively, is considered to be a moderate intake; the type of beverage has been established not to be important when defining moderation. Particular attention is often focused on the U-or J-shaped curve which also suggests that light to moderate drinking produces a protective effect. Such an inverse relationship indicates a reduction of risk for both light and moderate consumers and a higher risk not only for hard drinkers, but also for non-consumers.

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“…Precisely why alcoholism predisposes individuals to invasive pneumococcal disease, including endocarditis, remains unclear. An array of immunologic defects were described in alcoholics, any of which might contribute to sustained bacteraemia and risk of endocardial infection; these defects include leukocyte defects such as impaired chemotaxis, a dysfunctional reticuloendothelial system due to impaired expression of Fc receptors, and impaired delayed-type hypersensitivity [3,4]. Most researchers consider that the effect of alcoholism on host immunity is multifactorial, stemming not only from various immunologic defects as described but also from malnutrition and the propensity to aspiration.…”

Section: Discussionmentioning

confidence: 96%