GPR183 antagonism reduces macrophage infiltration in influenza and SARS-CoV-2 infection.

"Conflict of interest: S. Bartlett reports an early career seed grant from the Mater Foundation, supporting the present study. H. Bielefeldt-Ohmann reports consulting fees from Paradigm Biopharma, Queensland University of Technology and Colorado State University, outside the submitted work. M.J. Sweet reports grants from National Health and Medical Research Council of Australia, outside the submitted work. K. Bisht reports grants from the American Society of Hematology (ASH) Global Research Award, and Translational Research Institute-Mater Research LINC grant, Mater Foundation, outside the submitted work. Y. Yang reports grants from Mater Foundation, supporting the present study. J-P. Lévesque reports grants from National Health and Medical Research Council, and US Department of Defense; and royalties or licences from GlycoMimetics Inc., outside the submitted work. M.M. Rosenkilde reports support for the animal studies and breeding in Denmark of the mouse strain used in this study from Independent Research Fund Denmark; grants from Independent Research Fund Denmark, Novo Nordisk Foundation; donations from deceased Valter Alex Torbjørn Eichmuller (VAT Eichmuller)-2020-117043, and Kirsten and Freddy Johansens Foundation (KFJ) - 2017-112697; royalties from Antag Therapeutics and Bainan Biotech from patents made at the University of Copenhagen; travel support from Gordon Research Conference 2022; and is the co-founder of the following biotech companies: Antag Therapeutics, Bainan Biotech, Synklino, outside the submitted work. K.R. Short reports grants from National Health and Medical Research Council of Australia; and consulting fees from Sanofi, Novo Nordisk and Roche, outside the submitted work. K. Ronacher reports support for the present manuscript from Mater Foundation, Diabetes Australia, Australian Infectious Diseases Research Centre, Australian Respiratory Council; and grants from NIH R01 (5R01AI116039), outside the submitted work. All other authors have nothing to disclose."

"Author contributions: Conceptualisation: C.X. Foo, S. Bartlett, M.J. Sweet, K.R. Short, M.M. Rosenkilde, K. Ronacher. Methodology: K.Y. Chew, H. Bielefeldt-Ohmann, B.J. Arachchige, B. Matthews, S. Reed. Investigation: C.X. Foo, S. Bartlett, K.Y. Chew, M.D. Ngo, H. Bielefeldt-Ohmann, B.J. Arachchige, B. Matthews, S. Reed, R. Wang, C. Smith, L. Burr, K. Bisht, S. Shatunova, J.E. Sinclair, R. Parry, Y. Yang, J-P. Lévesque, A. Khromykh. Writing (original draft): C.X. Foo, S. Bartlett, K. Ronacher. Writing (review and editing): all authors. Funding acquisition: S. Bartlett, K.R. Short, M.M. Rosenkilde, K. Ronacher. Support statement: This study was supported by grants to K. Ronacher from the Mater Foundation, the Australian Respiratory Council, Diabetes Australia and the Australian Infectious Diseases Research Centre. S. Bartlett was supported by an early career seed grant from the Mater Foundation. The Translational Research Institute is supported by a grant from the Australian Government. The Danish Council for Independent Research I Medical Sciences supported M.M. Rosenkilde. M.J. Sweet, K.R. Short and J-P. Lévesque are supported by a National Health and Medical Research Council of Australia Investigator grant (1194406), Investigator Grant (2007919) and Senior Research Fellowship (1136130), respectively. Funding information for this article has been deposited with the Crossref Funder Registry."