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Deciphering rhinovirus-mediated macrophages impairment through the establishment of human induced pluripotent stem cells-derived macrophages

Project description

Mechanisms of virus-mediated macrophage response modulation

Viruses modulate myeloid cell responses, impairing macrophage phenotypes, and recent data suggest that this impairment can occur even without virus replication in these cells. Human rhinovirus (HRV) impairs macrophages’ responses to bacterial infection via downregulation of cytokine secretion. Understanding the mechanisms employed by viruses to modulate macrophages’ responses could offer therapeutic options to prevent virus-associated pathogenesis. Funded by the Marie Skłodowska-Curie Actions programme, the MacroRhino project aims to discover if HRV can replicate in alveolar macrophages and elucidate the HRV-mediated mechanisms of macrophage impairment. The researchers will develop a novel model of human lung alveolar macrophage-like cells derived from induced pluripotent stem cells to recapitulate organ physiology and the resident macrophage phenotype.

Objective

A growing body of evidence suggest that viruses can modulate myeloid cells responses leading to long term impairment of monocytes/macrophages phenotypes. Whereas for virus directly infecting macrophages, the long-term effects on these cells function and phenotype have been extensively studied, for virus infecting other cell types, the effects on macrophages have been overlooked. Yet, recent data suggest that virus-mediated modulation of macrophages can even occurred when the virus do not replicate in these cells. Indeed, viruses have broader ways to modulate the innate immune responses than the one identified in permissive cells. Understanding the mechanisms of action employed by viruses to modulate macrophages responses could not only provide possible targets to eliminate the infection, but also offer therapeutic options to prevent/avoid virus-associated pathogenesis.
Human rhinovirus (HRV) impairs macrophages’ responses upon secondary challenge with bacteria. The host laboratory identified arpin as a critical factor targeted by HRV to alter the phagocytic activity of macrophages and showed that HRV16-treated macrophages present a “paralysed” phenotype in terms of cytokine secretion. The precise mechanisms governing the reprogramming of the macrophages are however not fully elucidated. Furthermore, it is still unclear whether HRV needs to replicate within macrophages to reprogram their phenotype and functions. Therefore, my objectives are to decipher (i) if HRV can replicate in alveolar macrophages and (ii) what are the HRV-mediated mechanisms leading to impaired macrophages’ functions.
Moreover, the models employed to study macrophages present advantages but do not recapitulate organ physiology, which plays a key role on the resident macrophage phenotype. Therefore, I will develop a model of human lung alveolar macrophage-like cell (LAML) derived from induced pluripotent stem cells (h-iPSC) to answer the above-mentioned objectives.

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HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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Call for proposal

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(opens in new window) HORIZON-MSCA-2021-PF-01

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Coordinator

UNIVERSITE PARIS CITE
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 195 914,88
Address
85 BD SAINT GERMAIN
75006 PARIS
France

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Region
Ile-de-France Ile-de-France Paris
Activity type
Higher or Secondary Education Establishments
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Total cost

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