Research Topics

Cystic fibrosis and Gap junction

My research line is best summarized as "cell-cell and cell-matrix interactions in innate defense mechanisms in CF airway disease". As such, I am an active and recognized researcher in both the CF and the Gap Junction research fields. Over the years, we have shown that:

  • gap junctions contribute to the innate immune response of human airway epithelial cells,
  • abnormal composition of the airway luminal surface liquid facilitates chronic infection of CF airways;
  • irreversible adhesion of bacteria to the airway cell surface is caused by bacterial docking stations made of fibronectin and β1 integrin,
  • the guanine exchange factor Vav3, a Rho GTPases' activator, links CFTR to the formation of the luminal docking stations.

Our research aims are to understand the signaling pathways that promote apical fibronectin accumulation and determine at which stage of epithelial regeneration defect in these pathways occurs. We are investigating the molecular mechanisms by which defective CFTR increases Vav3 expression. We are also aiming to elucidate how an abnormal surface composition affects the integrity of the airway epithelium and promotes the exaggerated innate immune response that is characteristic of the CF lung disease.

Specific expertise

  • Gap junctions, connexins, pannexins
  • Epithelial transports, ion channels
  • Repair and regeneration of the airway epithelium
  • Innate immunity, host-pathogen interaction
  • Signal transduction
  • Cystic Fibrosis

Selected Publications

Badaoui M, Zoso A, Idris T, Bacchetta M, Simonin J, Lemeille S, Wehrle-Haller B, Chanson M. Vav3 mediates Pseudomonas aeruginosa adhesion to the Cystic Fibrosis airway epithelium. Cell Rep 32 (2020), 107842

Sofoluwe A, Zoso A, Bacchetta M, Lemeille S, Chanson M. Immune response of polarized cystic fibrosis airway epithelial cells infected with Influenza A virus. J Cyst Fibros S1569-1993 (2020), 30827-4

Sofoluwe A, Bacchetta M, Badaoui M, Kwak BR, Chanson M. ATP amplifies NADPH-dependent and -independent neutrophil extracellular trap formation. Sci Rep 9 (2019), 16556

Losa D, Köhler T, Bellec J, Dudez T, Crespin S, Bacchetta M, Boulanger P, Hong SS, Morel S, Nguyen TH, van Delden C, Chanson M. Pseudomonas aeruginosa-induced apoptosis in airway epithelial cells is mediated by gap junctional communication in a JNK-dependent manner. J Immunol 192 (2014), 4804-4812

Sarieddine MZ, Scheckenbach KE, Foglia B, Maass K, Garcia I, Kwak BR, Chanson M. Connexin43 modulates neutrophil recruitment to the lung.J Cell Mol Med 13 (2009), 4560-4570

November 6, 2020
  Host response to pathogens