Disruption of Physiological Rhythms Persist Following Cessation of Cigarette Smoke Exposure in Mice

Vanderstocken, Gilles; Marrow, Jade P.; Allwood, Melissa A.; Stämpfli, Martin R.; Simpson, Jeremy A.

doi:10.3389/fphys.2020.501383

Cited by 6 publications

(7 citation statements)

References 54 publications

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“…While studies have demonstrated that cannabis smoke increases locomotion in rats [ 40 ], our model appears to have the opposite effect, potentially due to the opposing effects of prolonged time in the smoke-filled exposure chamber. TPM in the chamber was seen to be at similar levels to those seen in tobacco smoke studies using the same system [ 25 , 39 ], which may also contribute to the tobacco smoke-like behavioural phenotype we observed. While TPM alone contributes to lung inflammation [ 41 , 42 ], cannabis smoke contains a myriad of other chemical components, cannabinoids, and reactive oxygen species, which can alter cellular and immunological functions.…”

Section: Discussionsupporting

confidence: 77%

“…Our cannabis smoke-exposure model was effective at delivering cannabis smoke to mice. Within the exposure chamber, mice displayed common symptoms of smoke exposure seen in our previous tobacco studies but tolerated smoke exposure well [ 25 , 39 ]. While studies have demonstrated that cannabis smoke increases locomotion in rats [ 40 ], our model appears to have the opposite effect, potentially due to the opposing effects of prolonged time in the smoke-filled exposure chamber.…”

Section: Discussionmentioning

confidence: 99%

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Development and validation of a mouse model of contemporary cannabis smoke exposure

et al. 2021

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Cannabis is widely used for both recreational and medicinal purposes. Inhalation of combusted cannabis smoke is the most common mode of drug consumption, exposing the lungs to the pharmacologically active ingredients, including tetrahydrocannabinol (THC) and cannabidiol (CBD). While the relationship between cannabis smoke exposure and compromised respiratory health has yet to be sufficiently defined, previous investigations suggest that cannabis smoke may dysregulate pulmonary immunity. Presently, there exists few pre-clinical animal models that have been extensively validated for contemporary cannabis smoke exposure. To address this need, we developed a mouse model with readouts of total particular matter, serum cannabinoid and carboxyhemoglobin levels, lung cellular responses, and immune mediator production.Using a commercially available smoke exposure system and a cannabis source material of documented THC/CBD composition, we exposed mice to a total particulate matter of 698.89 (sd=66.09) µg·L−1 and demonstrate increases in serum cannabinoids and carboxyhemoglobin. We demonstrate that cannabis smoke modulates immune cell populations and mediators in both male and female BALB/c mice. This modulation is highlighted by increases in airway and lung tissue macrophage populations, including tissue-resident alveolar macrophages, monocyte-derived alveolar macrophages, and interstitial macrophage subpopulations. No changes in airway or lung tissue infiltration of neutrophils were observed. Immune mediator analysis indicated significant upregulation of MDC, TARC, and VEGF within the lung tissue of cannabis smoke exposed mice. This accessible and reproducible smoke exposure model provides a foundation to explore the impact of chronic cannabis exposures and/or co-exposures with pathogens of clinical relevance, such as influenza.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Development and validation of a mouse model of contemporary cannabis smoke exposure

et al. 2021

Self Cite

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“…While studies have demonstrated that cannabis smoke increases locomotion in rats 37 , our model appears to have the opposite effect, potentially due to the opposing effects of prolonged time in the smoke-filled exposure chamber. TPM in the chamber was seen to be at similar levels to those seen in tobacco smoke studies using the same system 25,36 , which may also contribute to the tobacco smoke-like behavioural phenotype we observed. In our post-exposure analysis, we found elevated levels of COHb, THC, and carboxy-THC across the sexes that decreased 60 minutes post exposure (Fig.…”

Section: Discussionsupporting

confidence: 76%

“…Our cannabis smoke exposure model was effective at delivering cannabis smoke to mice. Within the exposure chamber, mice displayed common symptoms of smoke exposure seen in our previous tobacco studies but tolerated smoke exposure well 25,36 . While studies have demonstrated that cannabis smoke increases locomotion in rats 37 , our model appears to have the opposite effect, potentially due to the opposing effects of prolonged time in the smoke-filled exposure chamber.…”

Section: Discussionmentioning

confidence: 82%

Development and validation of a mouse model of contemporary cannabis smoke exposure

Fantauzzi

Cass

McGrath

et al. 2021

Preprint

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Cannabis is widely used for both recreational and medicinal purposes. Inhalation of combusted cannabis smoke is the most common mode of drug consumption, exposing the lungs to the pharmacologically active ingredients, including tetrahydrocannabinol (THC) and cannabidiol (CBD). While the relationship between cannabis smoke exposure and compromised respiratory health has yet to be sufficiently defined, previous investigations suggest that cannabis smoke may dysregulate pulmonary immunity. Presently, there exists few pre-clinical animal models that have been extensively validated for contemporary cannabis smoke exposure. To address this need, we developed a mouse model with readouts of total particular matter, serum cannabinoid and carboxyhemoglobin levels, lung cellular responses, and immune mediator production. Using a commercially available smoke exposure system and a cannabis source material of documented THC/CBD composition, we exposed mice to a total particulate matter of 698.89 (SD = 66.09) μg/L and demonstrate increases in serum cannabinoids and carboxyhemoglobin. We demonstrate that cannabis smoke modulates immune cell populations and mediators in both male and female BALB/c mice. This modulation is highlighted by increases in airway and lung tissue macrophage populations, including tissue-resident alveolar macrophages, monocyte-derived alveolar macrophages, and interstitial macrophage subpopulations. No changes in airway or lung tissue infiltration of neutrophils were observed. Immune mediator analysis indicated significant upregulation of MDC, TARC, and VEGF within the lung tissue of cannabis smoke exposed mice. This accessible and reproducible smoke exposure model provides a foundation to explore the impact of chronic cannabis exposures and/or co-exposures with pathogens of clinical relevance, such as influenza.

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“…Knockout mice for Rev-erbα, an important circadian clock component, showed increased susceptibility to inflammation after exposure to cigarette smoke-derived PM ( 228 ). Natural physiological rhythms of mice did not recover even 4 weeks after cessation of smoke exposure ( 239 ). Also, altered methylation of the Clock gene was found in blood cells of free-living birds in dependence of PM10 exposure ( 202 ).…”

Section: Connection Of Air Pollution Circadian Clock Dysregulation An...mentioning

confidence: 99%

Redox Regulatory Changes of Circadian Rhythm by the Environmental Risk Factors Traffic Noise and Air Pollution

Daiber

Frenis

Kuntic

et al. 2022

Antioxidants & Redox Signaling

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Significance: Risk factors in the environment such as air pollution and traffic noise contribute to the development of chronic noncommunicable diseases. Recent Advances: Epidemiological data suggest that air pollution and traffic noise are associated with a higher risk for cardiovascular, metabolic, and mental disease, including hypertension, heart failure, myocardial infarction, diabetes, arrhythmia, stroke, neurodegeneration, depression, and anxiety disorders, mainly by activation of stress hormone signaling, inflammation, and oxidative stress. Critical Issues: We here provide an in-depth review on the impact of the environmental risk factors air pollution and traffic noise exposure (components of the external exposome) on cardiovascular health, with special emphasis on the role of environmentally triggered oxidative stress and dysregulation of the circadian clock. Also, a general introduction on the contribution of circadian rhythms to cardiovascular health and disease as well as a detailed mechanistic discussion of redox regulatory pathways of the circadian clock system is provided. Future Directions: Finally, we discuss the potential of preventive strategies or “chrono” therapy for cardioprotection. Antioxid. Redox Signal . 37, 679–703.

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Disruption of Physiological Rhythms Persist Following Cessation of Cigarette Smoke Exposure in Mice

Cited by 6 publications

References 54 publications

Development and validation of a mouse model of contemporary cannabis smoke exposure

Development and validation of a mouse model of contemporary cannabis smoke exposure

Development and validation of a mouse model of contemporary cannabis smoke exposure

Redox Regulatory Changes of Circadian Rhythm by the Environmental Risk Factors Traffic Noise and Air Pollution

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