RT Journal Article
SR Electronic
T1 Reduction of endogenous acetylcholine contributes to pulmonary inflammation in a model of emphysema in mice
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP P831
VO 40
IS Suppl 56
A1 Rosana Banzato
A1 Nathália Pinheiro
A1 Clarice Olivo
A1 Fernanda Santana
A1 Iolanda Tibério
A1 Vânia Prado
A1 Marco Antônio Prado
A1 Milton Martins
A1 Fernanda Lopes
A1 Carla Prado
YR 2012
UL http://erj.ersjournals.com/content/40/Suppl_56/P831.abstract
AB Emphysema is characterized by pulmonary inflammation and destruction. Acetylcholine (ACh) regulates inflammation due to the activity of the cholinergic anti-inflammatory system in several diseases and ACh release depends on neurotransmitter storage in synaptic vesicles mediated by the vesicular acetylcholine transporter (VAChT). Aim: To investigate the role of the cholinergic system on emphysema in mice with reduced levels of ACh release. Methods: Mice with decreased expression of VAChT (VAChT KDHOM 70%) (HOM) and littermate wild-type mice (WT) received intranasal elastase or saline on day 0. On day 28, pulmonary mechanics, bronchoalveolar lavage fluid (BALF), mean linear intercept (Lm), elastic and collagen fibers in alveolar septa were evaluated. Results: WT-treated elastase animals presented a reduction in tissue elastance (Htis) and an increase in Lm, total cells and macrophages in BALF, and collagen and elastic fibers in lung parenchyma compared to saline groups (p<0.05). The HOM-treated elastase animals presented high values of total cells, macrophages, lymphocytes and neutrophils in BALF compared to WT-treated elastase group (P<0.05). There were no differences between WT-treated elastase and HOM-treated elastase groups in Htis, Lm, collagen and elastic fibers content. Conclusions: Reduction of endogenous ACh worsens pulmonary inflammation in mice with emphysema without changing pulmonary function and remodeling, suggesting that inflammation per se is not the major determinant of pulmonary function in this model. Our results suggest however a major role of the cholinergic anti-inflammatory system in the control of inflammatory response induced by elastase.