Effects of second hand cigarette smoke exposure on alveolarization in C57Bl/6J mice pups - 09/05/26

Smoking during pregnancy is a significant risk factor for intrauterine growth restriction and respiratory diseases. However, mechanisms involved in this process are not well defined.

The objective are to evaluate the effects of prenatal tobacco exposure on early postnatal lung development.

Mice were randomly divided into two groups: control (CTL) or second hand tobacco exposure (CS) group starting 5 days before mating and during gestation. Lung morphometry, immunofluorescence (IF), and 3D positive EPCAM+ cells culture were performed at 10 and 21 days of postnatal life (P10 and P21). IF markers were SpC+ for AT2, Krt8 for pre-alveolar differentiate intermediate cell (pre-ADI) and Ki67 for cell proliferation.

Weight, height and Lee index were lower in CS compared to CTL group. Morphometric study showed an increase of mean linear intercept in CS animals at P10 ( p < 0.05) without any differences at P21. IF analysis showed a decrease of AT2 cells (SpC+/Dapi) in the CS group compared with CTL at P21. Proliferation of AT2 (Spc+/Ki67 + ) were significantly increased in CS group compared to control at P10 and P21. Number of pre-ADI cells (Spc+/Krt8 + ) was significantly increased in CS group at P10 but not at P21. Alveolospheres analysis showed a significant increase of Epcam+ cells number in CS group at P10 compared to control ( P < 0.05).

Antenatal CS exposure disturbs growth and early lung development. Higher proliferation of Epcam+ cells at P10 and increased differentiation allows an alveolarization catch-up on P21. Further studies are needed to better characterize the alveolar niche after antenatal CS exposure.