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Published on: January 10, 2015
Adolescent nicotine: deficits in immune function
H A Navarro1, P V Basta, F J Seidler
1Center for Chemistry and Life Sciences, Research Triangle Institute, Research Triangle Park, NC 27709, USA.
Insights
Adolescent nicotine exposure disrupts T-cell function, leading to lasting immune deficiencies. This study highlights the adolescent immune system
Area of Science:
- Immunology
- Neuroscience
- Developmental Biology
Background:
- Maternal smoking during pregnancy alters offspring immune function.
- Prenatal nicotine exposure causes lasting T-lymphocyte deficiencies via cholinergic stimulation.
- Adolescence is a critical period for immune system development and the onset of smoking.
Purpose of the Study:
- To investigate if adolescent nicotine exposure impacts T-cell immune responses.
- To determine the vulnerability of the adolescent immune system to nicotine-induced mis-programming.
Main Methods:
- Adolescent rats received nicotine infusions (25 ng/ml) from postnatal day 30 to 47.5.
- Splenocyte mitogenic responses to Concanavalin A were assessed at PN45 and PN80.
- Nicotine levels mimicked those in human smokers and transdermal nicotine users.
Main Results:
- No immune deficiencies were observed immediately after nicotine exposure (PN45).
- Significant decreases in T-cell mitogenic responses were evident one month post-exposure (PN80).
- Deficits in T-cell function occurred at both suboptimal and optimal Concanavalin A concentrations.
Conclusions:
- The adolescent immune system is vulnerable to nicotine-induced disruption of T-cell function.
- Nicotine exposure during adolescence can lead to long-term immune system deficits.
- These findings suggest adolescent smoking may have lasting consequences on immune health.
Abstract:
Maternal cigarette smoking during pregnancy is known to alter immune function in the offspring and recent studies with animals indicate that prenatal nicotine exposure leads to lasting deficiencies in T-lymphocyte mitogenic responses, likely through excessive cholinergic stimulation during a critical stage of development. The current study was conducted to determine if the vulnerable period for nicotine-induced mis-programming of immune responses extends into adolescence, the stage at which most smokers begin tobacco use. Adolescent rats were given nicotine via osmotic minipump infusions on postnatal days (PN) 30-47.5, using a regimen that produces plasma levels (25 ng/ml) of nicotine similar to those in smokers or in users of transdermal nicotine patches. Toward the end of the infusion period (PN45) and 1 month after termination of nicotine exposure (PN80), we examined the mitogenic responses of splenocytes to Concanavalin A. Although no deficiencies were seen on PN45, there were robust decreases in mitogenic responses on PN80, with deficits apparent at both suboptimal and optimal concentrations of Concanavalin A. These results indicate that the adolescent immune system is vulnerable to nicotine-induced disruption of T-cell function.
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