scholarly journals Sex differences in lymphoid follicles in COPD airways

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Anthony Tam ◽  
Naoya Tanabe ◽  
Andrew Churg ◽  
Joanne L. Wright ◽  
James C. Hogg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Male Mice ◽  
Cross Sectional ◽  
Lymphoid Aggregate ◽  
Lymphoid Follicles ◽  
Female Mice ◽  
Female Sex Hormones ◽  
Lymphoid Aggregates

Abstract Background Female smokers have increased risk for chronic obstructive pulmonary disease (COPD) compared with male smokers who have a similar history of cigarette smoke exposure. Tertiary lymphoid follicles are often found in the lungs of patients with severe COPD but sex-related differences have not been previously investigated. We determined the impact of female sex hormones on chronic cigarette smoke-induced expression of lymphoid aggregates in mice with COPD-like pathologies. Methods Lymphoid aggregate counts, total aggregate cross-sectional area and foamy macrophage counts were determined morphometrically in male, female, and ovariectomized mice exposed to air or cigarette smoke for 6 months. B-cell activating factor (BAFF) protein expression and markers of oxidative stress were evaluated in mouse lung tissues by immunofluorescence staining and gene expression analyses. Quantitative histology was performed on lung tissue sections of human COPD lungs to evaluate follicle formation. Results Lymphoid follicle and foamy macrophage counts as well as the total follicle cross-sectional area were differentially increased in lung tissues of female mice compared to male mice, and these differences were abolished by ovariectomy. These lymphoid aggregates were positive for CD45, CD20, CD21 and BAFF expression. Differential increases in Mmp12 and Cxcl2 gene expression correlated with an increase in foamy macrophages in parenchymal tissues of female but not male mice after smoke exposure. Parenchymal tissues from female mice failed to induce antioxidant-related genes in response to smoke exposure, and this effect was restored by ovariectomy. 3-nitrotyrosine, a stable marker of oxidative stress, positively correlated with Mmp12 and Cxcl2 gene expression. Hydrogen peroxide induced BAFF protein in mouse macrophage cell line. In human lung tissues, female smokers with severe COPD demonstrated increased numbers of lymphoid follicles compared with males. Conclusions Chronic smoke exposure increases the risk of lymphoid aggregate formation in female mice compared with male mice, which is mediated female sex hormones and BAFF expression in an oxidative environment.

scholarly journals Mouse Protocadherin-1 Gene Expression Is Regulated by Cigarette Smoke Exposure In Vivo

PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e98197 ◽  
Author(s):  
Henk Koning ◽  
Antoon J. M. van Oosterhout ◽  
Uilke Brouwer ◽  
Lisette E. den Boef ◽  
Renée Gras ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Exposure In Vivo

scholarly journals Total particulate matter concentration skews cigarette smoke's gene expression profile

2016 ◽  
Vol 2 (4) ◽  
pp. 00029-2016 ◽  
Author(s):  
Anna Dvorkin-Gheva ◽  
Gilles Vanderstocken ◽  
Ali Önder Yildirim ◽  
Corry-Anke Brandsma ◽  
Ma'en Obeidat ◽  
...  
Keyword(s):  
Gene Expression ◽  
Particulate Matter ◽  
Cigarette Smoke ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
Total Particulate Matter ◽  
Xenobiotic Detoxification

Exposure of small animals to cigarette smoke is widely used as a model to study the pathogenesis of chronic obstructive pulmonary disease. However, protocols and exposure systems utilised vary substantially and it is unclear how these different systems compare.We analysed the gene expression profile of six publically available murine datasets from different cigarette smoke-exposure systems and related the gene signatures to three clinical cohorts.234 genes significantly regulated by cigarette smoke in at least one model were used to construct a 55-gene network containing 17 clusters. Increasing numbers of differentially regulated clusters were associated with higher total particulate matter concentrations in the different datasets. Low total particulate matter-induced genes mainly related to xenobiotic/detoxification responses, while higher total particulate matter activated immune/inflammatory processes in addition to xenobiotic/detoxification responses. To translate these observations to the clinic, we analysed the regulation of the revealed network in three human cohorts. Similar to mice, we observed marked differences in the number of regulated clusters between the cohorts. These differences were not determined by pack-year.Although none of the experimental models exhibited a complete alignment with any of the human cohorts, some exposure systems showed higher resemblance. Thus, depending on the cohort, clinically observed changes in gene expression may be mirrored more closely by specific cigarette smoke exposure systems. This study emphasises the need for careful validation of animal models.

scholarly journals Impact of maternal cigarette smoke exposure on brain inflammation and oxidative stress in male mice offspring

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Yik Lung Chan ◽  
Sonia Saad ◽  
Carol Pollock ◽  
Brian Oliver ◽  
Ibrahim Al-Odat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Brain Inflammation ◽  
Cigarette Smoke Exposure ◽  
Male Mice ◽  
And Oxidative Stress

scholarly journals Impact of acute exposure to cigarette smoke on airway gene expression

2018 ◽  
Vol 50 (9) ◽  
pp. 705-713 ◽  
Author(s):  
E. Billatos ◽  
A. Faiz ◽  
Y. Gesthalter ◽  
A. LeClerc ◽  
Y. O. Alekseyev ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Lung Cancer ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Acute Exposure ◽  
Cigarette Smoke Exposure ◽  
Airway Epithelial ◽  
Long Term Effects ◽  
Chronic Smoking

Background: Understanding effects of acute smoke exposure (ASE) on airway epithelial gene expression and their relationship with the effects of chronic smoke exposure may provide biological insights into the development of smoking-related respiratory diseases. Methods: Bronchial airway epithelial cell brushings were collected from 63 individuals without recent cigarette smoke exposure and before and 24 h after smoking three cigarettes. RNA from these samples was profiled on Affymetrix Human Gene 1.0 ST microarrays. Results: We identified 91 genes differentially expressed 24 h after ASE (false discovery rate < 0.25). ASE induced genes involved in xenobiotic metabolism, oxidative stress, and inflammation and repressed genes related to cilium morphogenesis and cell cycle. While many genes altered by ASE are altered similarly in chronic smokers, metallothionein genes are induced by ASE and suppressed in chronic smokers. Metallothioneins are also suppressed in current and former smokers with lung cancer relative to those without lung cancer. Conclusions: Acute exposure to as little as three cigarettes and chronic smoking induce largely concordant changes in airway epithelial gene expression. Differences in short-term and long-term effects of smoking on metallothionein expression and their relationship to lung cancer requires further study given these enzymes’ role in the oxidative stress response.

scholarly journals Sexually Dimorphic Responses to a High-Refined Carbohydrate Diet in a Nonalcoholic Fatty Liver Disease Mouse Model

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 16-16
Author(s):  
Michael Daniels ◽  
Chun Liu ◽  
Kang-Quan Hu ◽  
Xiang-Dong Wang
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Hepatic Steatosis ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Sexually Dimorphic ◽  
Male Mice ◽  
Carbohydrate Diet ◽  
Nonalcoholic Fatty Liver ◽  
Female Mice

Abstract Objectives Nonalcoholic fatty liver disease (NAFLD) incidence and prevalence have been reported to be higher in men than women, however, the effects of sexual dimorphism on NAFLD risk and progression have not been adequately examined. Our lab has previously shown that a liquid high-refined carbohydrate diet (HRCD) induced more severe hepatic steatosis compared to an isocaloric high fat diet in male mice. Also, HRCD-induced reduction in sirtuin 1 (SIRT1), an NAD-dependent deacetylase protein, has previously been implicated in NAFLD pathogenesis. Therefore, we investigated whether there were sexually dimorphic responses to a liquid high-refined carbohydrate diet (HRCD) in male and female, wildtype and SIRT1-deficient mice. Methods Male and female 10–12-week-old wildtype (SIRT1 +/+: n = 12; M = 6, F = 6) and mice carrying a heterozygous H355Y SIRT1 point mutation (SIRT1 +/y: n = 14; M = 7, F = 7) were both fed a HRCD (Lieber-DeCarli liquid diet supplemented with maltose dextrin; 47% energy from refined carbohydrate, Dyets, #710,260) for 5 weeks and 9 weeks. Hepatic gene expression was examined using qRT-PCR. Plasma ALT (alanine transaminase) and hepatic MDA (malondialdehyde) levels were determined using colorimetric assay kits. Hepatic steatosis scoring was conducted by analyzing Hematoxylin and Eosin (H&E) stains. Results 9 weeks of HRCD induced significantly less hepatic steatosis in female mice irrespective of genotype compared to male mice as determined by grading of H&E stains (P &lt; 0.05). Furthermore, liver expression of several fatty acid oxidation genes (CPT1, ACOX1) was significantly higher in females (P &lt; 0.05), which potentially suggests increased fatty acid oxidation. Additionally, female mice had significantly increased antioxidant gene expression (GPX4, SOD1, SOD2, Catalase) and significantly lower hepatic MDA (P &lt; 0.05), which indicate an increased capacity to mitigate oxidative stress. Lastly, plasma ALT levels were significantly lower in females compared to males after 9 weeks of HRCD (P &lt; 0.05). Conclusions Collectively, these data indicate that female mice are moderately protected against HRCD-induced NAFLD compared to male mice, potentially through increased hepatic fatty acid oxidation and superior mitigation of oxidative stress due to increased antioxidant system gene expression in the liver. Funding Sources HNRCA, USDA/ARS Grants.

Mouse anococcygeus muscle: sexual dimorphism and responsiveness to sex hormones

1997 ◽  
Vol 152 (2) ◽  
pp. 229-237 ◽  
Author(s):  
Y Fukazawa ◽  
T Iguchi ◽  
H A Bern
Keyword(s):  
Sexual Dimorphism ◽  
Oestrogen Receptor ◽  
Strain Differences ◽  
Neonatal Exposure ◽  
Thin Sheets ◽  
Male Mice ◽  
Cross Sectional ◽  
Female Mice ◽  
Anococcygeus Muscle ◽  
Icr Mice

Abstract The anococcygeus muscle (AcM) is one of a pair of thin sheets of smooth muscle inserting on the rectum, having a tendinous origin largely on sacral vertebrae. The cross-sectional area of AcM in the juxtarectal region in 90-day-old male mice was significantly larger than that in females of three strains: BALB/cCrgl, ICR/Jcl and C57BL/Tw. The AcM area in female mice showed strain differences: BALB/c>ICR>C57BL. Five daily injections of testosterone into newborn ICR mice from the day of birth significantly increased the areas of AcM in both sexes at 30 days of age, but five daily injections of oestradiol-17β (OE) decreased them. The AcM area in 60-day-old ICR male mice castrated at 30 days of age was significantly smaller than in intact males, and that in ovariectomized females was significantly larger than in intact females. In both sexes, implantation of a testosterone pellet (12 mg) into gonadectomized mice on the day of gonadectomy stimulated the growth of AcM, and implantation of an OE pellet (12 mg) inhibited the growth of AcM. The AcM in both ICR and C57BL strains showed positive androgen receptor and oestrogen receptor immunostaining at 15 days. Female ICR mice exposed neonatally to diethylstilboestrol (DES) had significantly larger AcM than controls; ovariectomy at 30 days of age did not change the AcM area in 60-day-old DES-exposed mice. However, male mice exposed neonatally to DES had significantly smaller AcM than controls; castration at 30 days of age nullified this inhibition. These results suggest that both androgen and oestrogen play an important role in sexual dimorphism of the mouse AcM. Neonatal exposure to DES (but not to oestradiol) had an irreversible stimulatory effect on the AcM area in female mice. Journal of Endocrinology (1997) 152, 229–237

scholarly journals Low birthweight of children is positively associated with mother’s prenatal tobacco smoke exposure in Shanghai: a cross-sectional study

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Ruiping Wang ◽  
Ting Sun ◽  
Qiong Yang ◽  
Qing Yang ◽  
Jian Wang ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Smoking Prevalence ◽  
Low Birthweight ◽  
Cross Sectional Study ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Cross Sectional ◽  
Shs Exposure ◽  
The Mean

Abstract Introduction Low birthweight (LBW) is a significant public health issue, and maternal smoking is the most prevalent preventable cause of LBW. But there is limited evidence on association of LBW among children and cigarette smoke exposure in mothers in China. In this cross-sectional study, we try to explore if the LBW in children is positively associated with mothers’ prenatal cigarette smoke exposure. Methods We selected 8, 586 mothers and their singleton children in 2018 in Songjiang district, Shanghai. Birthweight of children and gestational weeks of mother was identified by birth records in the hospital, we classified mothers’ prenatal cigarette smoke status into the first-hand smoke (FHS) exposure and the second-hand smoke (SHS) exposure. We use SAS 9.1.3 software to calculate the prevalence of children’s LBW and the prevalence of mothers’ prenatal cigarette smoke exposure including FHS and SHS. Chi-square test and logistic regression were used to analyze the difference. Results In 8, 586 women, The prenatal FHS and SHS exposure prevalence was 0.9 and 20.8%, respectively. The mean birthweight of children was 3315.5 g with a standard deviation of 497.2 g, the mean birthweight was 167.7 g and 66.1 g lower in children born to mothers with prenatally FHS and SHS exposure compared with those children whose mother were not exposed, respectively. The children’s LBW prevalence was 4.7% in this study. By comparing with children whose mother were not exposed, the LBW prevalence was higher among children whose mother were prenatally exposed to FHS [OR (Odds Ratios) = 2.91, 95% confidence interval (CI) (1.49, 5.68)], and SHS [OR = 2.35, 95% CI (1.90, 2.89)]. Conclusions Children’s LBW is positively associated with mothers’ prenatal tobacco smoke exposure both for FHS and SHS. So implementing tobacco control measures is crucial to lower smoking prevalence among women, and decrease smoking prevalence of their family members as well as work fellows.

scholarly journals Identification of gene expression signature for cigarette smoke exposure response—from man to mouse

2015 ◽  
Vol 34 (12) ◽  
pp. 1200-1211 ◽  
Author(s):  
F Martin ◽  
M Talikka ◽  
J Hoeng ◽  
MC Peitsch
Keyword(s):  
Gene Expression ◽  
Cigarette Smoke ◽  
Whole Blood ◽  
Gene Expression Signature ◽  
High Specificity ◽  
Gene Signature ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Toxicant Exposure ◽  
Specificity And Sensitivity

Gene expression profiling data can be used in toxicology to assess both the level and impact of toxicant exposure, aligned with a vision of 21st century toxicology. Here, we present a whole blood-derived gene signature that can distinguish current smokers from either nonsmokers or former smokers with high specificity and sensitivity. Such a signature that can be measured in a surrogate tissue (whole blood) may help in monitoring smoking exposure as well as discontinuation of exposure when the primarily impacted tissue (e.g., lung) is not readily accessible. The signature consisted of LRRN3, SASH1, PALLD, RGL1, TNFRSF17, CDKN1C, IGJ, RRM2, ID3, SERPING1, and FUCA1. Several members of this signature have been previously described in the context of smoking. The signature translated well across species and could distinguish mice that were exposed to cigarette smoke from ones exposed to air only or had been withdrawn from cigarette smoke exposure. Finally, the small signature of only 11 genes could be converted into a polymerase chain reaction-based assay that could serve as a marker to monitor compliance with a smoking abstinence protocol.

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