Gestational nicotine exposure alone or in combination with ethanol down-modulates offspring immune function

Prenatal nicotine exposure has been shown to disrupt the development of a number of peripheral organs. In the current study, we examined the effects of gestational nicotine exposure, alone or in combination with ethanol exposure, on offspring immune function. Timed pregnant rats were treated with ei...

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Bibliographic Details
Published in:	International journal of immunopharmacology Vol. 22; no. 2; pp. 159 - 169
Main Authors:	Basta, P.V, Basham, K.B, Ross, W.P, Brust, M.E, Navarro, H.A
Format:	Journal Article
Language:	English
Published:	Oxford Elsevier Science 01-02-2000
Subjects:	Alcoholism and acute alcohol poisoning Animals b-adrenergic receptors Biological and medical sciences Concanavalin A - pharmacology Ethanol - toxicity Female Fetus - drug effects Gestational nicotine development Immune response Immune Tolerance - drug effects Lymphocyte Activation - drug effects Medical sciences nicotine Nicotine - toxicity Pregnancy Proliferation Rats Rats, Sprague-Dawley Receptors, Adrenergic, beta - analysis Receptors, Adrenergic, beta - drug effects Tobacco, tobacco smoking Toxicology Immune response Proliferation Gestational nicotine development Cell proliferation Ethanol Rat Toxicity Rodentia Oral administration Splenocyte Concanavalin A β-Adrenergic receptor Pregnancy Prenatal Vertebrata Biological fixation Mammalia Animal Lipopolysaccharide Subcutaneous administration Drug of abuse Lymphocyte Nicotine
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Summary:	Prenatal nicotine exposure has been shown to disrupt the development of a number of peripheral organs. In the current study, we examined the effects of gestational nicotine exposure, alone or in combination with ethanol exposure, on offspring immune function. Timed pregnant rats were treated with either nicotine (6 mg/kg/day) from gestation day 4–20 using subcutaneously implanted osmotic mini-pumps or ethanol administered in the drinking water (15% w/v) from gestation day 10–20. The combined exposure group received both treatments. The ability of offspring T and B cells to proliferate in response to nonspecific stimulation by Concanavalin A or lipopolysaccharide, respectively, was determined on postnatal days 9, 15, 22, 29, 64, and 86. Offspring splenocyte β 2-adrenoceptor binding was also measured. Nicotine or nicotine+ethanol suppressed splenocyte responsiveness to Concanavalin A or lipopolysaccharide which was similar in timing and magnitude to that seen with ethanol alone. Splenocytes from these groups remained subresponsive to stimulation well into adulthood. The combined drug treatment caused an overall reduction in spleen β-adrenergic receptor binding whereas the individual drug treatments did not alter the development of spleen β-adrenergic receptors. Our results indicate that prenatal nicotine exposure can cause long-term suppression of the proliferative response of offspring immune cells. Moreover, the effects of nicotine+ethanol may cause more severe deficits in adulthood.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23
ISSN:	0192-0561 1879-3495
DOI:	10.1016/S0192-0561(99)00074-0