Inflammation is a central feature of numerous respiratory diseases. In the lung, inflammation must be resolved efficiently while preventing tissue damage that could impair gas exchange. The airways must also discriminate between the vast amount of non-threatening antigens and the much rarer pathogenic signals. If this fine balance is disturbed, it can lead on one hand to increase susceptibility to infections like pneumonia or on the other hand to the damage of lung tissue and compromised respiratory functions. Therefore, inflammation is an underlying or major contributing factor to numerous respiratory diseases like asthma, cystic fibrosis (CF), chronic obstructive pulmonary diseases (COPD) and lung cancer.
A number of cellular receptors are involved in the recognition of pathogen-associated molecular patterns by the host, including Toll-like receptors (TLRs) and Nod-like receptors (NLRs). These receptors provide a crucial link between the sensing of pathogens and the elaboration of the immune response. As they are key modulators of immune function, they provide a novel therapeutic approach to prevent, increase or modulate the immune response in human inflammatory diseases.
The aim of my research program is to understand the role of intracellular signaling pathways in controlling the synthesis of inflammatory mediators following activation of the innate immune response that can alter the structure and function of the airways.
Specific research objectives:
- To understand the molecular mechanisms triggering pulmonary exacerbations in Cystic fibrosis
- Use artificial intelligence to analyze experimental (-omics) data from biological material and clinical data from the Biobanque québécoise de la COVID-19 (BQC19) to define the molecular endophenotypes associated with the different clinical trajectories of COVID-19
- Signaling pathways regulating the synthesis of Th1 or Th2 promoting cytokines by airway epithelial cells in response to infection
- Identifying key pathways bridging the innate and adaptive immune systems in dendritic cells
- Flagellin-mediated chemokine production by airway epithelial cells.
RI-MUHC, Block E
1001 Decarie Blvd.
Montreal QC H4A 3J1
Tel: 514-934-1934 Ext. 76205 (lab)
Tel: 514-934-1934 Ext. 76394 (office)
Tel: 514-934-1934 Ext. 76172 (admin)
E-Mail: simon.rousseau [at] mcgill.ca