Nicotine‐induced neuroepithelial cell changes in young rabbits: A preliminary communication

Chen, M. F.; Diotallevi, M; Kimizuka, Goro; King, Malcolm; Wang, N. S.

doi:10.1002/ppul.1950010606

Cited by 11 publications

(2 citation statements)

References 16 publications

(2 reference statements)

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“…Both maternal nicotine treatment and cigarette smoke exposure disrupt alveolarization in rats, guinea pigs, mice, and rhesus monkeys [66,111-115]. Of note, a recent report by Singh and colleagues demonstrated that maternal smoking decreased cAMP in the lung tissue of the offspring [66].…”

Section: Discussionmentioning

confidence: 99%

Maternal smoking and the retinoid pathway in the developing lung

et al. 2012

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BackgroundMaternal smoking is a risk factor for pediatric lung disease, including asthma. Animal models suggest that maternal smoking causes defective alveolarization in the offspring. Retinoic acid signaling modulates both lung development and postnatal immune function. Thus, abnormalities in this pathway could mediate maternal smoking effects. We tested whether maternal smoking disrupts retinoic acid pathway expression and functioning in a murine model.MethodsFemale C57Bl/6 mice with/without mainstream cigarette smoke exposure (3 research cigarettes a day, 5 days a week) were mated to nonsmoking males. Cigarette smoke exposure continued throughout the pregnancy and after parturition. Lung tissue from the offspring was examined by mean linear intercept analysis and by quantitative PCR. Cell culture experiments using the type II cell-like cell line, A549, tested whether lipid-soluble cigarette smoke components affected binding and activation of retinoic acid response elements in vitro.ResultsCompared to tobacco-naïve mice, juvenile mice with tobacco toxin exposure had significantly (P < 0.05) increased mean linear intercepts, consistent with an alveolarization defect. Tobacco toxin exposure significantly (P < 0.05) decreased mRNA and protein expression of retinoic acid signaling pathway elements, including retinoic acid receptor alpha and retinoic acid receptor beta, with the greatest number of changes observed between postnatal days 3–5. Lipid-soluble cigarette smoke components significantly (P < 0.05) decreased retinoic acid-induced binding and activation of the retinoic acid receptor response element in A549 cells.ConclusionsA murine model of maternal cigarette smoking causes abnormal alveolarization in association with altered retinoic acid pathway element expression in the offspring. An in vitro cell culture model shows that lipid-soluble components of cigarette smoke decrease retinoic acid response element activation. It is feasible that disruption of retinoic acid signaling contributes to the pediatric lung dysfunction caused by maternal smoking.

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Section: Discussionmentioning

confidence: 99%

Maternal smoking and the retinoid pathway in the developing lung

et al. 2012

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“…In conditions such as chronic obstructive pulmonary disease (COPD) and emphysema, cigarette smoking has been associated with increased numbers of PNEC and NEB [5,6]. In addition, some animal models have shown hyperplasia of PNEC/NEB and increased expression of NE peptides after exposure to cigarette smoke or its components [7,8]. Many of the peptides or bioactive amines secreted from the PNEC may play a role in the inflammatory processes of airway diseases as growth factors, immunoregulators or neurotransmitters [9].…”

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Increased serum levels of chromogranin A in male smokers with airway obstruction

Sørhaug

Hveem²,

Steinshamn³

2006

European Respiratory Journal

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The neuroendocrine (NE) system may play an important role in smoking-induced airway diseases. The aim of the present study was to examine the relationship between serum levels of the general NE marker chromogranin A (CgA) and smoking habits, respiratory symptoms and lung function.The study population consisted of never-smokers with normal lung function, smokers with normal lung function and smokers with airway obstruction who were randomly selected from the lung study of the Nord-Trøndelag Health Study (HUNT). Serum CgA was determined in 151, 138 and 116 subjects, respectively. All subjects were seronegative for Helicobacter pylori.Male smokers with airway obstruction had significantly higher serum CgA levels (median 3.70 nmol?L -1 (interquartile range 3.10-5.15)) than both smokers with normal lung function (3.00 nmol?L -1 (2.50-3.67)) and never-smokers with normal lung function (2.90 nmol?L -1 (2.57-3.30)).The elevated levels of CgA correlated with the degree of airway obstruction. Moreover, the presence of respiratory symptoms and chronic bronchitis among male smokers were associated with increased serum CgA levels. Females had CgA levels similar to male smokers independent of smoking status and lung function. Elevated serum chromogranin A levels in subjects with airway obstruction and respiratory symptoms may represent neuroendocrine activation in inflammatory or remodelling processes in the lung.

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Human fetal lung changes associated with maternal smoking during pregnancy

Chen

Kimizuka

Wang

1987

Pediatric Pulmonology

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Pulmonary impairment in the offspring of smoking mothers is well documented by epidemiologic studies. The morphologic bases for the functional impairment are largely unexplored. We studied 17 infant lungs obtained at autopsy, ten from smoking (group 1) and seven from nonsmoking (group 2) mothers, by light (LM), transmission (TEM), and scanning electron microscopy (SEM). By LM, the alveolar mean linear intercept was similar in both groups; the total lung volume and alveolar surface area increased with the increase in gestational age in all lungs studied. By SEM, the sizes of the neuroepithelial bodies (NEB) were larger in group 1 than in group 2. By SEM and TEM, ciliated cells were increased, but the amount of dense core granules was decreased, in the NEB of the smoking group. Maternal smoking during pregnancy appears to alter the size and cellular composition of fetal NEB. The detailed mechanisms of the alteration in NEB and their implications are unclear from this study and needed further clarification.

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Nicotine‐induced neuroepithelial cell changes in young rabbits: A preliminary communication

Cited by 11 publications

References 16 publications

Maternal smoking and the retinoid pathway in the developing lung

Maternal smoking and the retinoid pathway in the developing lung

Increased serum levels of chromogranin A in male smokers with airway obstruction

Human fetal lung changes associated with maternal smoking during pregnancy

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