Diminished Proliferative Response of Con A‐blast Cells to Interleukin 2 in Adult Rats Exposed to Ethanol in Utero

Norman, Dean C.; Mei, Chao; Castle, Steven; Zuylen, J. E.; Taylor, Anna N.

doi:10.1111/j.1530-0277.1989.tb00286.x

Cited by 49 publications

(8 citation statements)

References 15 publications

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“…Consistent with this latter possibility, we found reduced lymph node lymphocyte proliferative responses to Con A in PAE animals overall on day 7, and in PAE animals in the Adj/NA condition on day 16. These data replicate and extend previous results from our laboratory (Weinberg and Jerrells, 1991) and others (Ewald and Frost, 1987; Norman et al, 1989) demonstrating reduced splenic and thymic lymphocyte proliferative responses to mitogens, as well as reduced thymic and splenic T-cell responses to a secondary stimulation by IL-2. Blunted proliferation at induction of arthritis could reduce cytokine production and recruitment of cells to the joints, thus delaying arthritis onset.…”

Section: Discussionsupporting

confidence: 91%

“…Delayed thymic ontogeny, decreased total numbers of splenic and thymic T cells, decreased thymus weight, size, and cell counts, and suppressed B cell development have all been observed in fetuses and newborns exposed to alcohol in utero (Ewald and Walden, 1988; Ewald and Huang, 1990; Clausing et al, 1996; Moscatello et al, 1999). These changes may persist into adolescence and adulthood, and additional immune deficits, including altered responses to the intestinal parasite, Trichinella spiralis and deficits in mitogen-induced lymphocyte and lymphoblast cell proliferation to mitogens, may be revealed as the animal matures (Ewald and Frost, 1987; Ewald, 1989; Norman et al, 1989; Redei et al, 1989; Gottesfeld et al, 1990; Weinberg and Jerrells, 1991; Steven et al, 1992; Redei et al, 1993; Giberson and Blakley, 1994; Clausing et al, 1996; Seelig et al, 1996; Jerrells and Weinberg, 1998; Taylor et al, 1999). Moreover, exposure to stressors, including cold stress and chronic intermittent stress, may exacerbate immune deficits in PAE compared to control animals (Giberson and Weinberg, 1995; Giberson et al, 1997).…”

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confidence: 99%

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Prenatal alcohol exposure alters the course and severity of adjuvant-induced arthritis in female rats

Zhang

Bach

et al. 2012

Brain, Behavior, and Immunity

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Prenatal alcohol exposure (PAE) has adverse effects on the development of numerous physiological systems, including the hypothalamic-pituitary-adrenal (HPA) axis and the immune system. HPA hyper-responsiveness and impairments in immune competence have been demonstrated. The present study investigated immune function in PAE females utilizing an adjuvant-induced arthritis (AA) model, widely used as a model of human rheumatoid arthritis. Given the effects of PAE on HPA and immune function, and the known interaction between HPA and immune systems in arthritis, we hypothesized that PAE females would have heightened autoimmune responses, resulting in increased severity of arthritis, compared to controls, and that altered HPA activity might play a role in the immune system changes observed. The data demonstrate, for the first time, an adverse effect of PAE on the course and severity of AA in adulthood, indicating an important long-term alteration in functional immune status. Although overall, across prenatal treatments, adjuvant-injected animals gained less weight, and exhibited decreased thymus and increased adrenal weights, and increased basal levels of corticosterone and adrenocorticotropin, PAE females had a more prolonged course of disease and greater severity of inflammation compared to controls. In addition, PAE females exhibited blunted lymphocyte proliferative responses to concanavalin A and a greater increase in basal ACTH levels compared to controls during the induction phase, before any clinical signs of disease were apparent. These data suggest that prenatal alcohol exposure has both direct and indirect effects on inflammatory processes, altering both immune and HPA function, and likely, the normal interactions between these systems.

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Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 99%

Prenatal alcohol exposure alters the course and severity of adjuvant-induced arthritis in female rats

Zhang

Bach

et al. 2012

Brain, Behavior, and Immunity

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“…2, B and C). On days 14 and 21, E-PL offspring continued to weigh less than pairfed (PF-PL) and control offspring ( p's < 0.00 1) (Fig. 2B).…”

Section: Maternal and Offspring Weights During Lactationmentioning

confidence: 90%

“…Recent studies have demonstrated that prenatal ethanol exposure also causes a variety of immunological abnormalities. [13][14][15][16][17][18][19][20][21][22][23] To investigate the effects of ethanol exposure during immune system maturation, we exposed neonatal mice to ethanol via the breast milk. Because the early postnatal period is characterized by development and maturation of immunocompetence,27 we hypothesized that ethanol exposure restricted to this stage of development may result in an alteration in the surface antigen phenotype of splenic lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

Effect of Postnatal Ethanol Exposure on Expression of Differentiation Antigens of Murine Splenic Lymphocytes

Giberson

Blakley

1994

Alcoholism Clin & Exp Res

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Ethanol is a recognized immunosuppressive agent in the chronic alcoholic. However, the effects of ethanol exposure on the developing immune system have not been extensively investigated. This study evaluated the effects of early postnatal ethanol exposure, via breast milk, on splenic lymphocyte differentiation antigen expression in offspring reared by ethanol-fed mice. Maternal mice were fed a liquid diet containing 20% ethanol-derived calories during pregnancy (E-P), pregnancy and lactation (E-PL), or lactation (E-L). Ad libitum-fed (C) and pair-fed (PF) control groups, fed a control liquid diet, were included. Expression of differentiation antigens on splenic lymphocytes from 21-day-old offspring reared by females in 1 of the 3 ethanol exposure conditions was evaluated by flow cytometry. Offspring reared by E-P females had similar numbers of splenic lymphocytes as offspring reared by C and pair-fed during pregnancy (PF-P) females. In contrast, offspring reared by E-PL and E-L females had fewer splenic lymphocytes than both PF-PL and PF-L (respectively), and C offspring. The number of Thy 1.2+, CD4+, CD8+, and IgG+ (B-cell) splenic lymphocytes was reduced in E-PL and E-L offspring compared with PF and C offspring. E-P offspring had fewer CD4+ and IgG+ splenic lymphocytes than C, but not PF-P, offspring. The percentage of Thy 1.2+ splenic lymphocytes was significantly reduced among E-PL and E-L offspring compared with PF-PL and PF-L (respectively), and C offspring.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…The results of several studies have suggested that lymphocyte numbers and proliferation in responses to mitogen stimulation are reduced also in adult rats exposed to EtOH in utero (4, 12, 13, 19). Further, young adult mice exposed to EtOH in utero also have decreased contact hypersensitivity and graft versus host responses (14), suggesting the effects of ethanol exposure on immunity can last into adulthood.…”

Section: Introductionmentioning

confidence: 99%

Fetal Exposure to Ethanol Has Long-Term Effects on the Severity of Influenza Virus Infections

McGill

Meyerholz²,

Edsen-Moore³

et al. 2009

The Journal of Immunology

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Alcohol use by pregnant women is a significant public health issue despite well-described risks to the fetus including physical and intellectual growth retardation and malformations. Although clinical studies are limited, they suggest that in utero alcohol exposure also results in significant immune deficiencies in naive neonates. However, little is known about fetal alcohol exposure (FAE) effects on adult infections. Therefore, to determine the long-term effects of FAE on disease susceptibility and the adult immune system, we infected FAE adult mice with influenza virus. In this study, we demonstrate that mice exposed to ethanol during gestation and nursing exhibit enhanced disease severity as well as increased and sustained pulmonary viral titers following influenza virus infection. Secondary exposure to alcohol as an adult further exacerbates these effects. Moreover, we demonstrate that FAE mice have impaired adaptive immune responses, including decreased numbers of virus-specific pulmonary CD8 T cells, a decreased size and frequency of pulmonary B cell foci, and reduced production of influenza-specific Ab following influenza infection. Together, our results suggest that FAE induces significant and long-term defects in immunity and susceptibility to influenza virus infection and that FAE individuals could be at increased risk for severe and fatal respiratory infections.

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Diminished Proliferative Response of Con A‐blast Cells to Interleukin 2 in Adult Rats Exposed to Ethanol in Utero

Cited by 49 publications

References 15 publications

Prenatal alcohol exposure alters the course and severity of adjuvant-induced arthritis in female rats

Prenatal alcohol exposure alters the course and severity of adjuvant-induced arthritis in female rats

Effect of Postnatal Ethanol Exposure on Expression of Differentiation Antigens of Murine Splenic Lymphocytes

Fetal Exposure to Ethanol Has Long-Term Effects on the Severity of Influenza Virus Infections

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