The Air Pollution Impact to Maternal Mice and Offspring

Wang, Baoming

The Air Pollution Impact to Maternal Mice and Offspring

Wang, Baoming

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Publication Type:: Thesis
Issue Date:: 2021

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Field	Value	Language
dc.contributor.author	Wang, Baoming
dc.date.accessioned	2021-05-28T01:14:14Z
dc.date.available	2021-05-28T01:14:14Z
dc.date.issued	2021
dc.identifier.uri	http://hdl.handle.net/10453/149289
dc.description	University of Technology Sydney. Faculty of Science.	en_US.UTF-8
dc.description.abstract	Epidemiological studies have shown that maternal exposure to cigarette smoke and air pollution are two predominant 𝘪𝘯 𝘶𝘵𝘦𝘳𝘰 environmental toxicants which can increase the risk of developing multiple respiratory diseases in the offspring. The proposed mechanisms include reducing mitochondrial function and mitochondrial renewal mechanisms (mitophagy) and activating inflammasome and other inflammatory pathways. However, whether maternal smoking could induce the sex-dependent susceptibility in respiratory disorders and whether chronic low dose particulate matter (PM) exposure which is within the international standard could induce any transgenerational pulmonary disease has not been widely studied. Firstly, Female Balb/c mice (8 weeks) were exposed to cigarette smoke (SE) for 6 weeks prior to mating, during gestation and lactation. Half of the SE dams (mothers) were given L-Carnitine supplementation (1.5mM in drinking water, SE+LC) during gestation and lactation. Then, another Male Balb/c Mice (6 weeks, Animal Resources Centre, WA, Australia) batch was intranasally exposed to saline or traffic-related PM₁₀ (1 μg or 5 μg/day) for 3 weeks. Furthermore, the female BALB/c mice (6 weeks) were exposed to PM₂.₅ (PM₂.₅, 5 μg/day) or saline (SHAM) 6 weeks before pregnancy and during pregnancy and lactation; or for only 6 weeks before pregnancy (Cessation, 5 μg/day). Lung tissues from models were analysed. Results: Compared to female offspring, maternal SE significantly increased levels of inflammatory markers (phosphorylated(p)-extracellular signal-regulated kinase (ERK1,2), pp38 Mitogen-activated protein kinase (P38) MAPK, p-Mitogen-activated protein kinase (NF-kB). Three weeks of PM exposure (5 μg/day) significantly increased total macrophages and lymphocytes number in the bronchoalveolar lavage fluid (BALF) accompanied by increased levels of NLRP3 and Interlukin-1 (IL1-β). Chronic exposure to low dose PM significantly increased tissue elastance and damping during lung function tests, followed by increased leukocytes in the BALF, mitochondrial dysfunction, and airway remodelling, including alveolar membrane damage and increased collagen deposition. Maternal exposure to low dose PM also significantly increased tissue elastance and damping during lung function test followed by increased leukocytes in the BALF and mitochondrial dysfunction without airway remodelling. The mouse model of asthma induced by olvabumin (OVA) showed that maternal exposure to the low dose PM could significantly increase tissue elastance during lung function test in the offspring, suggesting the worse asthmatic symptoms. In conclusion, male offspring are more susceptible to the adverse effects of maternal smoking. Chronic exposure to the low dose PM could induce chronic obstructive pulmonary disease (COPD)-likes pathology in the dams and worsen asthmatic symptoms in the female offspring.	en_US.UTF-8
dc.format	Thesis (PhD)
dc.language.iso	en	en_US.UTF-8
dc.relation	https://opus.lib.uts.edu.au/bitstream/10453/149289/2/02Whole.pdf
dc.rights	The author owns the copyright in this thesis including all reproduction and reuse rights for the work. The work may not be altered without the permission of the copyright owner. Attribution is essential when quoting or paraphrasing from this thesis.
dc.rights	au.edu.uts.lib/ppc
dc.rights	info:eu-repo/semantics/openAccess
dc.title	The Air Pollution Impact to Maternal Mice and Offspring	en_US.UTF-8
dc.type	Thesis
utslib.copyright.status	open_access	*

Abstract:

Epidemiological studies have shown that maternal exposure to cigarette smoke and air pollution are two predominant 𝘪𝘯 𝘶𝘵𝘦𝘳𝘰 environmental toxicants which can increase the risk of developing multiple respiratory diseases in the offspring. The proposed mechanisms include reducing mitochondrial function and mitochondrial renewal mechanisms (mitophagy) and activating inflammasome and other inflammatory pathways. However, whether maternal smoking could induce the sex-dependent susceptibility in respiratory disorders and whether chronic low dose particulate matter (PM) exposure which is within the international standard could induce any transgenerational pulmonary disease has not been widely studied. Firstly, Female Balb/c mice (8 weeks) were exposed to cigarette smoke (SE) for 6 weeks prior to mating, during gestation and lactation. Half of the SE dams (mothers) were given L-Carnitine supplementation (1.5mM in drinking water, SE+LC) during gestation and lactation. Then, another Male Balb/c Mice (6 weeks, Animal Resources Centre, WA, Australia) batch was intranasally exposed to saline or traffic-related PM₁₀ (1 μg or 5 μg/day) for 3 weeks. Furthermore, the female BALB/c mice (6 weeks) were exposed to PM₂.₅ (PM₂.₅, 5 μg/day) or saline (SHAM) 6 weeks before pregnancy and during pregnancy and lactation; or for only 6 weeks before pregnancy (Cessation, 5 μg/day). Lung tissues from models were analysed. Results: Compared to female offspring, maternal SE significantly increased levels of inflammatory markers (phosphorylated(p)-extracellular signal-regulated kinase (ERK1,2), pp38 Mitogen-activated protein kinase (P38) MAPK, p-Mitogen-activated protein kinase (NF-kB). Three weeks of PM exposure (5 μg/day) significantly increased total macrophages and lymphocytes number in the bronchoalveolar lavage fluid (BALF) accompanied by increased levels of NLRP3 and Interlukin-1 (IL1-β). Chronic exposure to low dose PM significantly increased tissue elastance and damping during lung function tests, followed by increased leukocytes in the BALF, mitochondrial dysfunction, and airway remodelling, including alveolar membrane damage and increased collagen deposition. Maternal exposure to low dose PM also significantly increased tissue elastance and damping during lung function test followed by increased leukocytes in the BALF and mitochondrial dysfunction without airway remodelling. The mouse model of asthma induced by olvabumin (OVA) showed that maternal exposure to the low dose PM could significantly increase tissue elastance during lung function test in the offspring, suggesting the worse asthmatic symptoms. In conclusion, male offspring are more susceptible to the adverse effects of maternal smoking. Chronic exposure to the low dose PM could induce chronic obstructive pulmonary disease (COPD)-likes pathology in the dams and worsen asthmatic symptoms in the female offspring.

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http://hdl.handle.net/10453/149289