Changes in lymphocyte and macrophage subsets due to morphine and ethanol treatment during a retrovirus infection causing murine aids

Watson, Ronald R.; Prabhala, Rao; Darban, Hamid; Yahya, M. Danial; Smith, Thomas L.

doi:10.1016/0024-3205(88)90145-2

Cited by 50 publications

(10 citation statements)

References 12 publications

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“…Effects of morphine on lymphocyte subpopulations have been described, although a consensus has not been reached. For example, WATSON et al (1988) found a suppression of both T helper and T suppressor lymphocytes, while ARORA et al (1990) reported an increase in the T helper to T suppressor ratio following morphine treatment. We have found a modest increase in the percentage of T suppressor cells (PERRIT et al 1988).…”

Section: Morphinementioning

confidence: 94%

“…In the latter report, naltrexone administration prevented the increase in lethality from infection created by morphine exposure. WATSON et al (1988) employed a murine leukemic retrovirus model (which somewhat resembles HIV infection in the human) and demonstrated deleterious effects of chronic morphine treatment in a viral model as well.…”

Section: In Vivo Assessments Of Immune Function 1 Morphinementioning

confidence: 99%

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Opioids in Immunologic Processes

Bryant¹,

Holaday²

1993

Opioids II

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Section: Morphinementioning

confidence: 94%

Section: In Vivo Assessments Of Immune Function 1 Morphinementioning

confidence: 99%

Opioids in Immunologic Processes

Bryant¹,

Holaday²

1993

Opioids II

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“…The animals were allowed to become acclimated in a standard environment in the animal care room for 2 weeks before receiving any treatment. After this period, animals assigned to the virus-infected group were injected intraperitoneally with 0.1 mL LP-BM5 MuLV as described previously [8]. Control groups consisted of uninfected age-matched animals.…”

Section: Animalsmentioning

confidence: 99%

The effect of chronic retrovirus infection and immune dysfunction on the P-450-mediated activation of acetaminophen in mouse liver microsomes

Chow

Tang

et al. 1998

Biopharm. Drug Dispos.

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Acute viral infection has long been recognized to down‐regulate cytochrome P‐450 enzymes and subsequently to result in changes in the pharmacological and toxicological responses to xenobiotics. In our previous research, chronic retrovirus infection induced by inoculating a susceptible strain of mice with LP‐BM5 murine leukaemia virus (MuLV) was found to suppress acetaminophen (APAP) induced liver injury. In the present study, we aimed to examine the influence of chronic retrovirus infection and its associated immune dysfunction on the activities of a number of cytochrome P‐450 isozymes and the P‐450‐mediated activation of APAP in mouse liver microsomes. Liver microsomes prepared from female C57BL/6 mice at 8 and 16 weeks after LP‐BM5 MuLV inoculation as well as from age‐matched controls were used in the study. The catalytic activities of the cytochrome P‐450 isozymes 1A family and 2E1, catalysts for the activation of APAP, were measured in different microsomal preparations using O‐dealkylation of alkoxyresorufin homologues and oxidation of p ‐nitrophenol, respectively, as the metabolic markers. The formation of the reactive APAP metabolite trapped as glutathione conjugate in the microsomal preparations was also determined. We demonstrated that there were variable changes in total hepatic P‐450 levels and in the activities of a number of P‐450 isozymes in animals with chronic retrovirus infection and immune dysfunction. Such changes seemed to be dependent on the stage of the disease and to have resulted in increases or minimal changes in the rate of APAP activation in hepatic microsomes collected from this animal model. This suggests that the P‐450‐mediated activation of APAP was not down‐regulated in animals with chronic retrovirus infection. Enhanced elimination of APAP by detoxification metabolic pathways is more likely to be responsible for the increased resistance to APAP‐induced hepatotoxicity observed in our previous research in animals with chronic retrovirus infection. © 1998 John Wiley & Sons, Ltd.

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“…Another study showed a significantly higher rate of alcohol consumption among patients with more advanced HIV disease compared to asymptomatic HIV-infected individuals (16). Recent studies also showed that retroviral infections in the murine model also exacerbated the decreased host immune response to AIDS after retroviral infection (26,40). Since such a potential association exists between alcohol and HIV susceptibility or disease progression (16,26,27,35,37), it is possible that alcohol may compromise normal lymphocyte responses to HIV infection and may also have an inhibitory effect on the residual NK cell activities of lymphocytes from AIDS patients.…”

Section: Discussionmentioning

confidence: 99%

“…Natural killer cells PREVIOUS studies have shown that chronic alcohol consumption is associated with abnormalities of humoral (5,(8)(9)(10)21,22) and cellular immunity (6,11,13,14,39), including dysfunction of suppressor (11,12,15,40,41), helper (18), and cytotoxic lymphocyte activities (1,7,19,20,33,36) and production of soluble immune mediators (31). We have recently reported that lymphocytes from nonalcoholic, healthy donors precultured in vitro with different concentrations of alcohol manifest decreased levels of natural killer (NK), antibody-dependent cellular cytotoxic (ADCC), and lymphokine-activated killer (LAK) cell activities (23).…”

Section: Lymphocyte Proliferationmentioning

confidence: 99%

Selective effect of alcohol on cellular immune responses of lymphocytes from AIDS patients

Nair

Kumar

Kronfol

et al. 1994

Alcohol

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In this study we examined the in vitro effects of alcohol on the proliferative responses of lymphocytes from healthy donors and AIDS patients to a recombinant fusion peptide, env-gag, corresponding to portions of the gp41 envelope (env) and internal core (gag) proteins of HIV. The effects of alcohol (ETOH) on the natural killer (NK) cell activities of lymphocytes from healthy donors and patients with AIDS were also investigated. Peripheral blood mononuclear cells from both normal donors and AIDS patients produced significant levels of lymphocyte proliferative responses to the HIV env-gag peptide; however, these responses were significantly higher in patients with AIDS, showing the specificity of the response. The env-gag-induced proliferative responses of lymphocytes from normal subjects were significantly suppressed when cultures contained only higher levels of ETOH (0.2% and 0.3%), whereas ETOH even at a lower level (0.1%) produced significant suppression of the env-gag-induced proliferation of lymphocytes only from AIDS patients. Direct addition of ETOH at concentrations of 0.1%, 0.2%, and 0.3% to cultures of lymphocytes from normal donors and NK target cells did not produce significant suppression of NK cell activities. However, ETOH at concentrations of 0.2% and 0.3% significantly suppressed the NK activities of lymphocytes from AIDS patients, and the suppressive effect was observed at all E:T cell ratios examined. Control peptide from the Escherichia coli expression vector did not produce any significant effect on lymphocyte proliferative responses or NK activity of both normal donors and AIDS patients.(ABSTRACT TRUNCATED AT 250 WORDS)

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Changes in lymphocyte and macrophage subsets due to morphine and ethanol treatment during a retrovirus infection causing murine aids

Cited by 50 publications

References 12 publications

Opioids in Immunologic Processes

Opioids in Immunologic Processes

The effect of chronic retrovirus infection and immune dysfunction on the P-450-mediated activation of acetaminophen in mouse liver microsomes

Selective effect of alcohol on cellular immune responses of lymphocytes from AIDS patients

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