Passive cigarette smoke exposure induces airway hyperreactivity in guinea-pig: Role of inflammation

1988 ◽  
Vol 20 ◽  
pp. 121
Author(s):  
L. Daffonchio ◽  
A. Hernandez ◽  
G. Clavenna ◽  
G. Zuccari ◽  
C. Omini
Keyword(s):  
Guinea Pig ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Airway Hyperreactivity ◽  
Cigarette Smoke Exposure

Airway Responsiveness to Intravenous and Inhaled Acetylcholine in the Guinea Pig after Cigarette Smoke Exposure

1987 ◽  
Vol 136 (5) ◽  
pp. 1158-1162 ◽  
Author(s):  
Alan L. James ◽  
Peter Dirks ◽  
Hitoshi Ohtaka ◽  
R. Robert Schellenberg ◽  
James C. Hogg
Keyword(s):  
Guinea Pig ◽  
Cigarette Smoke ◽  
Airway Responsiveness ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure

scholarly journals Systemic effects of cigarette smoke exposure in the guinea pig

2006 ◽  
Vol 100 (7) ◽  
pp. 1186-1194 ◽  
Author(s):  
Esther Ardite ◽  
Víctor I. Peinado ◽  
Roberto A. Rabinovich ◽  
José C. Fernández-Checa ◽  
Josep Roca ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Systemic Effects

Sidestream cigarette smoke exposure and airway reactivity during early life

1994 ◽  
Vol 77 (4) ◽  
pp. 1868-1874 ◽  
Author(s):  
Y. L. Lai ◽  
A. Thacker ◽  
C. G. Gairola
Keyword(s):  
Cigarette Smoke ◽  
Early Life ◽  
Airway Hyperreactivity ◽  
Cigarette Smoke Exposure ◽  
Bronchial Reactivity ◽  
Group 4 ◽  
Maximal Expiratory Flow ◽  
Expiratory Flow ◽  
Guinea Pig Model

We established a guinea pig model to investigate effects of in utero and neonatal exposure to sidestream cigarette smoke (SSCS) on bronchial reactivity during early life. Animals were divided into four groups: 1) room air/room air, 2) sham/sham, 3) SSCS/room air, and 4) SSCS/SSCS. Pregnant and neonatal animals of group 1 breathed room air and those of group 2 were sham treated. Pregnant animals of both groups 3 and 4 as well as neonates of group 4 were exposed to SSCS. SSCS exposure was limited to between days 28 and 55 of pregnancy and days 8 and 24 of the neonatal period. Bronchial response to acetylcholine (ACh) and substance P (SP) were determined in very young animals at 25 days of age. Maximal expiratory flow was used as an index of airway dimension. SP, but not ACh, induced a significantly larger decrease in peak maximal expiratory flow in group 4, indicating an important role of neonatal SSCS exposure in augmenting bronchial response to SP. To further investigate the role of tachykinins in cigarette smoke-induced changes in bronchial reactivity, four additional groups (the same as above) of neonates were pretreated with capsaicin to deplete tachykinins. In the SSCS/SSCS group, SP-induced airway hyperreactivity was abolished by capsaicin pretreatment. Furthermore, in all four groups, capsaicin pretreatment abolished the bronchial response to SP but not the response to ACh. In additional very young animals, acute SSCS caused a nonsignificant increase in bronchial response to SP. These results indicate that chronic neonatal SSCS exposure induces bronchial hyperreactivity to SP; this hyperreactivity is abolished by capsaicin pretreatment.

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.

scholarly journals The Role of Endoplasmic Reticulum Stress in Emphysema Results from Cigarette Smoke Exposure

2011 ◽  
Vol 28 (4) ◽  
pp. 725-732 ◽  
Author(s):  
Guixiang Gan ◽  
Ruicheng Hu ◽  
Aiguo Dai ◽  
Shuangxiang Tan ◽  
Qing Ouyang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure
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