scholarly journals Exposure to Cigarette Smoke Enhances Pneumococcal Transmission Among Littermates in an Infant Mouse Model

2021 ◽  
Vol 11 ◽  
Author(s):  
Daichi Murakami ◽  
Masamitsu Kono ◽  
Denisa Nanushaj ◽  
Fumie Kaneko ◽  
Tonia Zangari ◽  
...  
Keyword(s):  
Environmental Factors ◽  
Mouse Model ◽  
Cigarette Smoke ◽  
Close Contact ◽  
Smoke Exposure ◽  
Mucosal Barrier ◽  
Cigarette Smoke Exposure ◽  
New Host ◽  
Infant Mouse ◽  
The Impact

Streptococcus pneumoniae, one of the most common commensal pathogens among children, is spread by close contact in daycare centers or within a family. Host innate immune responses and bacterial virulence factors promote pneumococcal transmission. However, investigations into the effects of environmental factors on transmission have been limited. Passive smoking, a great concern for children’s health, has been reported to exacerbate pneumococcal diseases. Here, we describe the effect of cigarette smoke exposure on an infant mouse model of pneumococcal transmission. Our findings reveal that the effect of cigarette smoke exposure significantly promotes pneumococcal transmission by enhancing bacterial shedding from the colonized host and by increasing susceptibility to pneumococcal colonization in the new host, both of which are critical steps of transmission. Local inflammation, followed by mucosal changes (such as mucus hypersecretion and disruption of the mucosal barrier), are important underlying mechanisms for promotion of transmission by smoke exposure. These effects were attributable to the constituents of cigarette smoke rather than smoke itself. These findings provide the first experimental evidence of the impact of environmental factors on pneumococcal transmission and the mechanism of pathogenesis.

scholarly journals Chronic Cigarette Smoke Exposure Primes NK Cell Activation in a Mouse Model of Chronic Obstructive Pulmonary Disease

2010 ◽  
Vol 184 (8) ◽  
pp. 4460-4469 ◽  
Author(s):  
Gregory T. Motz ◽  
Bryan L. Eppert ◽  
Brian W. Wortham ◽  
Robyn M. Amos-Kroohs ◽  
Jennifer L. Flury ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Mouse Model ◽  
Pulmonary Disease ◽  
Cigarette Smoke ◽  
Cell Activation ◽  
Nk Cell ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

scholarly journals Cigarette exposure induces changes in maternal vascular function in a pregnant mouse model

2010 ◽  
Vol 298 (5) ◽  
pp. R1249-R1256 ◽  
Author(s):  
Robin E. Gandley ◽  
Arun Jeyabalan ◽  
Ketaki Desai ◽  
Stacy McGonigal ◽  
Jennifer Rohland ◽  
...  
Keyword(s):  
Mouse Model ◽  
Cigarette Smoke ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Smoke Exposure ◽  
Renal Arteries ◽  
Growth Restriction ◽  
Whole Body ◽  
Cigarette Smoke Exposure ◽  
Pregnant Mice

Smoking is associated with multiple adverse pregnancy outcomes, including fetal growth restriction. The objective of this study was to determine whether cigarette smoke exposure during pregnancy in a mouse model affects the functional properties of maternal uterine, mesenteric, and renal arteries as a possible mechanism for growth restriction. C57Bl/CJ mice were exposed to whole body sidestream smoke for 4 h/day. Smoke particle exposure was increased from day 4 of gestation until late pregnancy ( day 16–19), with mean total suspended particle levels of 63 mg/m3, representative of moderate-to-heavy smoking in humans. Uterine, mesenteric, and renal arteries from late-pregnant and virgin mice were isolated and studied in a pressure-arteriograph system ( n = 23). Plasma cotinine was measured by ELISA. Fetal weights were significantly reduced in smoke-exposed compared with control fetuses (0.88 ± 0.1 vs. 1.0 ± 0.08 g, P < 0.02), while litter sizes were not different. Endothelium-mediated relaxation responses to methacholine were significantly impaired in both the uterine and mesenteric vasculature of pregnant mice exposed to cigarette smoke during gestation. This difference was not apparent in isolated renal arteries from pregnant mice exposed to cigarette smoke; however, relaxation was significantly reduced in renal arteries from smoke-exposed virgin mice. In conclusion, we found that passive cigarette smoke exposure is associated with impaired vascular relaxation of uterine and mesenteric arteries in pregnant mice. Functional maternal vascular perturbations during pregnancy, specifically impaired peripheral and uterine vasodilation, may contribute to a mechanism by which smoking results in fetal growth restriction.

scholarly journals Long-Term Cigarette Smoke Exposure in a Mouse Model of Ciliated Epithelial Cell Function

2010 ◽  
Vol 43 (6) ◽  
pp. 635-640 ◽  
Author(s):  
Samantha M. Simet ◽  
Joseph H. Sisson ◽  
Jacqueline A. Pavlik ◽  
Jane M. DeVasure ◽  
Craig Boyer ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Mouse Model ◽  
Cigarette Smoke ◽  
Cell Function ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Ciliated Epithelial Cell

Cigarette Smoke Exposure Triggers Autophagy-Mediated Ovarian Follicle Loss in a Mouse Model.

2011 ◽  
Vol 85 (Suppl_1) ◽  
pp. 37-37
Author(s):  
Anne Marie Gannon ◽  
Martin Stampfli ◽  
Warren G. Foster
Keyword(s):  
Mouse Model ◽  
Cigarette Smoke ◽  
Ovarian Follicle ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure

scholarly journals Comparison and evaluation of two different methods to establish the cigarette smoke exposure mouse model of COPD

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Jiaze Shu ◽  
Defu Li ◽  
Haiping Ouyang ◽  
Junyi Huang ◽  
Zhen Long ◽  
...  
Keyword(s):  
Mouse Model ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure

scholarly journals The Impact of Maternal Cigarette Smoke Exposure in a Rodent Model on Renal Development in the Offspring

PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e103443 ◽  
Author(s):  
Ibrahim Al-Odat ◽  
Hui Chen ◽  
Yik Lung Chan ◽  
Sawiris Amgad ◽  
Muh Geot Wong ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Rodent Model ◽  
Cigarette Smoke Exposure ◽  
Renal Development ◽  
The Impact

T cell depletion protects against alveolar destruction due to chronic cigarette smoke exposure in mice

2013 ◽  
Vol 304 (5) ◽  
pp. L312-L323 ◽  
Author(s):  
Patricia L. Podolin ◽  
Joseph P. Foley ◽  
Donald C. Carpenter ◽  
Brian J. Bolognese ◽  
Gregory A. Logan ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Mouse Model ◽  
Cigarette Smoke ◽  
T Cell Responses ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
T Cell Depletion ◽  
Cell Responses

The role of T cells in chronic obstructive pulmonary disease (COPD) is not well understood. We have previously demonstrated that chronic cigarette smoke exposure can lead to the accumulation of CD4+ and CD8+ T cells in the alveolar airspaces in a mouse model of COPD, implicating these cells in disease pathogenesis. However, whether specific inhibition of T cell responses represents a therapeutic strategy has not been fully investigated. In this study inhibition of T cell responses through specific depleting antibodies, or the T cell immunosuppressant drug cyclosporin A, prevented airspace enlargement and neutrophil infiltration in a mouse model of chronic cigarette smoke exposure. Furthermore, individual inhibition of either CD4+ T helper or CD8+ T cytotoxic cells prevented airspace enlargement to a similar degree, implicating both T cell subsets as critical mediators of the adaptive immune response induced by cigarette smoke exposure. Importantly, T cell depletion resulted in significantly decreased levels of the Th17-associated cytokine IL-17A, and of caspase 3 and caspase 7 gene expression and activity, induced by cigarette smoke exposure. Finally, inhibition of T cell responses in a therapeutic manner also inhibited cigarette smoke-induced airspace enlargement, IL-17A expression, and neutrophil influx in mice. Together these data demonstrate for the first time that therapeutic inhibition of T cell responses may be efficacious in the treatment of COPD. Given that broad immunosuppression may be undesirable in COPD patients, this study provides proof-of-concept for more targeted approaches to inhibiting the role of T cells in emphysema development.

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