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Arpin is critical for phagocytosis in macrophages and is targeted by human rhinovirus
Author(s) -
Jubrail Jamil,
AfricanoGomez Kshanti,
Herit Floriane,
Mularski Anna,
Bourdoncle Pierre,
Oberg Lisa,
Israelsson Elisabeth,
Burgel PierreRegis,
Mayer Gaell,
Cunoosamy Danen M,
Kurian Nisha,
Niedergang Florence
Publication year - 2019
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201947963
Subject(s) - phagocytosis , phagosome , rhinovirus , macrophage , biology , microbiology and biotechnology , immunology , virus , in vitro , biochemistry
Human rhinovirus is a causative agent of severe exacerbations of chronic obstructive pulmonary disease (COPD). COPD is characterised by an increased number of alveolar macrophages with diminished phagocytic functions, but how rhinovirus infection affects macrophage function is still unknown. Here, we describe that human rhinovirus 16 impairs bacterial uptake and receptor‐mediated phagocytosis in macrophages. The stalled phagocytic cups contain accumulated F‐actin. Interestingly, we find that human rhinovirus 16 downregulates the expression of Arpin, a negative regulator of the Arp2/3 complex. Importantly, re‐expression of the protein rescues defective internalisation in human rhinovirus 16‐treated cells, demonstrating that Arpin is a key factor targeted to impair phagocytosis. We further show that Arpin is required for efficient uptake of multiple targets, for F‐actin cup formation and for successful phagosome completion in macrophages. Interestingly, Arpin is recruited to sites of membrane extension and phagosome closure. Thus, we identify Arpin as a central actin regulator during phagocytosis that it is targeted by human rhinovirus 16, allowing the virus to perturb bacterial internalisation and phagocytosis in macrophages.