in vivo services >> Lung inflammation models
Allergic asthma
This model has been validated with steroids, PDE type 4 and MAPK inhibitors and histamine scavenger proteins (Couillin et al., 2004).
Allergic asthma is characterized by airways hyperreactivity (AHR) which is assessed by whole body or invasive plethysmography. Furthermore, eosinophils, lymphocytes and other inflammatory cells are increased in the broncho-alveolar fluid (BALF) and into lung tissue due to increased cytokines and chemokines, which are quantified by ELISA.
Lungs are homogenized for measurement of eosinophil peroxidase (EPO) activity, and cell infiltration into lung and mucus productions are determined by histological assessment.
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Emphysema
(Couillin et al 2007)
Acute lung injury (ALI)
We have established an endotoxin induced model (Ryffel et al., 2005a; Schnyder-Candrian et al., 2005, Togbe et al 2006) as well as an intestinal ischemia/reperfusion lung injury in mice (Soares et al Shock, 2010).
LPS induced acute lung injury (ALI) is assessed by whole body plethysmography; BALF: neutrophils, total and differential cells counts recruited into lung, cytokines quantification. Lungs are homogenized for measurement of eosinophil peroxidase (EPO) activity, cell infiltration into lung is determined by histological assessment.
Smoke
CPOD is a major public health issue with chronic obstructive inflammation leading to respiratory insufficiency. Cigarette smoke exposure models in part CPOD, we have established this model in mice (Doz E J Immunol 2008).
Chronic bronchitis and fibrosis (COPD)
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Bleomycin induced lung inflammation and fibrosis is assessed at day 1 and day 10, respectively.
For the inflammatory response: cell count in the bronchoalveolar lavage fluid (BALF); neutrophil in lung (MPO) and cytokines/ chemokines and tissue inhibitor metalloproteinase-1 (TIMP-1) in lung homogenate are determined. For the analysis of lung fibrosis collagen, TIMP-1 and histology and immunostaining in the lung are performed. (Gasse et al., 2011)
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