ISSN 2756-3375
African Journal of Immunology Research Vol. 1 (1) pp. 006-011, October, 2014. © International Scholars Journals
Full Length Research Paper
Maternal nicotine presentation changed representation of laminin α 5 in lung tissue of infant mice
*Mohammed E. Ahmed, Ali Hatami and Golshifteh Khamenei
Department of Anatomy and Cell Biology, School of Medicine, Payame Noor University, Iran.
E-mail: [email protected]
Accepted 14 September, 2014
Abstract
Maternal smoking has been clearly demonstrated to be associated with increased health problems in infants and children. Nicotine is a chemical substance with high level of toxicity. It crosses through the placenta and accumulates in the developing organs of fetus. Previous investigation indicated that maternal nicotine exposures induce decreased fibronectin expression in lung parenchyma. In this study, the effect of maternal nicotine exposure on laminin expression of the newborn mice lungs has been evaluated. 24 female pregnant Balb/C mice were divided randomly into four groups as follows: Experimental Group 1 (Exp D1); received 3 mg/kg nicotine intra peritoneal injection (IP) from gestational day 7 (GD7) to the last day of pregnancy, Experimental Group 2 (Exp D14); received 3 mg/kg nicotine from GD7 to post natal day 14, Groups 3 and 4; as sham control groups (Sha-Con) received the same volume (3 mg/kg) of normal saline parallel to experimental groups. At the end of exposure times, all the newborns were anesthetized, their lungs were removed and prepared for immunohistochemical method and real-time polymerase chain reaction. Our finding indicated that laminin alpha 5(Lama5) mRNA expression in the lung of newborn in the nicotine treated Exp D1 decreased by 0.63 fold but increased in Exp D14 by 1.57 fold comparing to Sh-Con groups. Lama5 immunoreactivity was not similar in different parts of the lungs including alveoli and bronchiole, having a significant increase in the experimental groups in contrast to the Sh-Con groups. These data also indicate that maternal nicotine exposure may induce abnormal laminin expression which may cause defects in lung function during life time.
Key words: Laminin, lung, nicotine, mouse.