{"id":1885,"date":"2021-01-20T17:18:10","date_gmt":"2021-01-20T16:18:10","guid":{"rendered":"https:\/\/wordpress-test.app.u-pariscite.fr\/sdv\/?page_id=1885"},"modified":"2021-01-20T17:18:10","modified_gmt":"2021-01-20T16:18:10","slug":"immunite-innee-et-defense-pulmonaire-anti-infectieuse","status":"publish","type":"page","link":"https:\/\/wordpress-test.app.u-pariscite.fr\/sdv\/immunite-innee-et-defense-pulmonaire-anti-infectieuse\/","title":{"rendered":"Immunit\u00e9 inn\u00e9e et d\u00e9fense pulmonaire anti-infectieuse"},"content":{"rendered":"

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This team is directed by Jean-Michel Sallenave, in the INSERM UMR1152 unit.<\/strong><\/h4>\n
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PRESENTATION<\/strong><\/h3>\n

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At the surface of the epithelium and pulmonary alveoli, epithelial cells and innate immune cells (alveolar macrophages, MDSCs, NK cells, Innate lymphoid cells\/ILCs, eosinophils..) interact, \u00a0through the production of surfactant, regulatory cytokines and antimicrobial molecules, to ensure a non- inflammatory regulatory phenotype.<\/p>\n

After infective or toxic stimuli exposure, these cells participate in a network to organize pro-inflammatory responses and to engage adaptive immunity to contain the aggression, foster tissue repair, and to insure the return to haemostasis.<\/p>\n

Our research group (Team 3, INSERM U1152, Facult\u00e9 de M\u00e9decine, H\u00f4pital Bichat, Paris) is mostly interested in the innate mechanisms put in place in these processes and in the dysregulation of these control mechanisms.<\/p>\n

Relatedly, we have a keen interest in translational medicine since a dysregulation of these control mechanisms could potentially explain the pathophysiology of some inflammatory disorders (chronic obstructive pulmonary diseases\/COPD, cystic fibrosis, ventilator-associated pneumonia..)<\/p>\n

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Four main areas of investigation are currently being pursued in our team\u00a0:<\/strong><\/h3>\n

1) Study in vitro <\/em>and in vivo <\/em>of the role of Pseudomonas aeruginosa <\/em>infections (an opportunistic pathogen in pulmonary nosocomial infection and in cystic fibrosis) in exacerbations of chronic lung diseases, including cystic fibrosis. \u00a0<\/p>\n

2) In vitro <\/em>and in vivo <\/em>study of the mechanisms through which Influenza <\/em>virus, a pathogen responsible for lung infections in seasonal flu or pandemic episodes can favour bacterial super-infections and induce disease exacerbations in chronic lung diseases.<\/p>\n

\u00a03) Study of host-pathogen interactions in COVID-19<\/p>\n

\u00a04) Investigation of the molecular mechanisms of action of nanoparticles in the lung, in isolation or in conjunction with lung pathogens (S. aureus, P.aeruginosa, Influenza <\/em>virus\u2026<\/em>), and their use as potential adjuvants in vaccination protocols.<\/p>\n

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Technological tools : the molecular processes, techniques, reagents, signalling pathways studied and used in this context include\u00a0:<\/strong><\/h3>\n

-mechanisms of Pathogen Associate Molecular Pattern\/PAMP receptors activation, phagocytic processes, signal transduction \u00a0pathways\u00a0; role of epithelial type 2 serine proteases (TTSPs) during Influenza infection\u00a0; interactions between microbial virulence factors, innate immune\u00a0 receptors\u00a0 and epithelial channels (eg CFTR) ; study of endogenous antimicrobial mol\u00e9cules\u00a0; use of recombinant adenovirus vectors in over-expression protocols\u00a0; in<\/em> vivo <\/em>rodent infection models\u00a0; \u00a0RT-qPCR\u00a0; flow cytometry\u00a0; immuno-histochemistry\u00a0; proteomics.<\/p>\n

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Recent Selected publications<\/strong><\/h3>\n

\u00a0-Saint-Criq V et al. Thorax<\/em>, 2018; 73:49-61\u00a0; -Villeret B et al. ACS Nano<\/em>. 2018;12:1188-1202\u00a0; \u00a0-Bastaert F et al. Front Immunol<\/em>. 2018;9:1675.\u00a0; -Sanchez-Guzman D et al. Biomaterials<\/em>. 2019;217:119308 ; \u00a0-Villeret B et al. Front Immunol<\/em>. 2020, 11:117 ; \u00a0-Sallenave JM,\u00a0Guillot L. \u00a0Front Immunol<\/em>. 2020;11:1229\u00a0; -Kheir S et al. \u00a0BioRxiv preprint : https:\/\/doi.org\/10.1101\/2020.07.22.214684<\/a><\/p>\n

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Current Research Funding\u00a0:<\/strong><\/h3>\n