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Perinatal Nicotine Exposure Disrupts Hematopoietic Stem Cell Development and Elevates Influenza Susceptibility in
T Cool1,2, A Rodriguez Y Baena1,2, Mge Rommel2
1Program in Biomedical Science and Engineering, University of California Santa Cruz, Santa Cruz, CA 95064, USA.
Insights
Perinatal nicotine exposure impairs immune cell development, leading to lifelong susceptibility to respiratory infections like influenza in adulthood. This occurs due to lasting changes in immune cell function, not just numbers.
Area of Science:
- Immunology
- Developmental Biology
- Respiratory Medicine
Background:
- Tobacco use during pregnancy poses risks to maternal and fetal health.
- Offspring of smoking mothers exhibit increased respiratory disease frequency and severity.
- Altered immune systems, potentially from epigenetically maladaptive hematopoietic stem cells (HSCs), may underlie this vulnerability.
Purpose of the Study:
- To investigate the long-term effects of perinatal nicotine exposure on immune cell development and function.
- To elucidate the mechanisms by which prenatal smoke exposure increases susceptibility to respiratory infections.
Main Methods:
- Perinatal nicotine exposure (PNE) in a model system.
- Analysis of hematopoietic stem cells (HSCs) and immune cell populations.
- Assessment of immune response and disease severity upon influenza A virus challenge in adulthood.
Main Results:
- PNE altered HSC establishment and fetal-derived non-traditional tissue immune cells, with no change in circulating immune cells.
- Immune cell suppression persisted weeks after PNE cessation.
- PNE led to increased susceptibility and severity of influenza A infection in adulthood, linked to altered lung immune cells.
Conclusions:
- Perinatal exposures can permanently impair immune function by affecting hematopoietic establishment.
- Nicotine exposure during development creates lasting cellular deficits, weakening defenses against respiratory pathogens throughout life.
Abstract:
Tobacco use during pregnancy has many deleterious health consequences for not only the smoking mother, but also on the unborn fetus. Children of smoking mothers are reported to have higher frequency and severity of respiratory diseases later in life; however, the mechanisms driving this increased vulnerability are not clearly understood. One potential cause of increased disease susceptibility is an altered immune system, originating in epigenetically maladaptive hematopoietic stem cells (HSCs). Here, we show that perinatal nicotine exposure (PNE) alters the establishment of HSCs and fetal-derived non-traditional tissue immune cells, with no alterations in circulating immune cell numbers. Suppression of HSCs and lung immune cells persisted for weeks after PNE had ceased. Strikingly, PNE led to increased disease susceptibility and severity upon challenge with influenza A virus in adulthood. This was associated with significant and highly selective alterations in lung immune cells, emphasizing the importance of cellular mechanisms in resilience to infections. Together, these experiments demonstrate that perinatal exposures that have deleterious consequences on hematopoietic establishment can impair immune function for life and identify the cellular mechanisms by which perinatal nicotine exposure predisposes the offspring to a weakened defense against respiratory pathogens.
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