Formation of immunodeficiency in newborn mice exposed to nicotine during intrauterine development.

Exposure to nicotine during intrauterine development leads to immunodeficiency manifested in inhibition of delayed-type hypersensitivity reaction and reduced number of antibody-producing cells forming in response to sheep erythrocytes in newborn mice. The number of splenic CFU in the bone marrow of newborn mice exposed to nicotine in utero is decreased compared to the control. By contrast, nicotine induced an increase in splenic CFU count in fetal liver. We concluded that nicotine modifying the hemopoietic microenvironment delayed the release of primitive precursors from fetal liver, which impaired colonization of fetal bone marrow and led to imbalance in the production of mature blood cell, including immune system cells.