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The role of TREM proteins in inflammatory lung disease (ALLOSERGON)
Start date: Feb 1, 2013, End date: Dec 23, 2016 PROJECT  FINISHED 

• Both asthma and pneumococcal infection independently affect millions of people world-wide causing significant mortality/morbidity and an associated high economic burden. It is indicated that pathogenesis in asthma is due to enhanced bacterial replication and invasiveness in the lung rather than a worsening of asthma itself.• The overall scientific objective is to combine established models of respiratory bacterial infection and house dust mite induced asthma in the mouse. This project is a new approach to identify the molecular mechanisms and the involvement of the novel surface receptor proteins TREM. Airway macrophages of the asthmatic lung will be analysed by high throughput flow cytometry, cell sorting, immunohistochemistry and cytokines measured by ELISA to identify innate immune alterations. It is indicated that the bacterial complications that occur in patients with underlying lung disease are due to an up-regulation of anti-inflammatory TREM-2 or a loss (via secretion) of membrane bound TREM-1. The main aim is to provide the key tools to reduce the severity of bacterial complications in asthma and identify targets for prophylactics/therapeutics.• High level supervision, specific training by experts in the set up of in vivo respiratory infection models, access to state-of-the-art equipment will enhance my position at the forefront of advances in this field. Strong interaction with other international researchers will enable transfer of knowledge and contribute to a sustainable network. The unique opportunity to attend leadership and management courses will allow me to reach scientific maturity and gain independence as a researcher.• This project fulfils all the ERA criteria and will notably contribute to Europe’s Vision 2020. The resultant publications in high impact factor journals will contribute to the worldwide recognition of European research and significantly strengthen the EU over US competitors in pulmonary chronic disease and infection.
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