Author

S. Bartlett

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Immunology· 3 Microbiology· 2

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 5 Research Focus:host-pathogen & immune response· 5 Organism:mouse· 5 Research Focus:cell type annotation· 2 Assay:proteomics· 2 Assay:bulk RNA-seq· 1 Assay:clinical cohort / trial· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

H. Bielefeldt-Ohmann· 4 shared K. Ronacher· 4 shared M. D. Ngo· 4 shared C. X. Foo· 3 shared M. M. Rosenkilde· 3 shared R. Sinha· 3 shared B. J. Arachchige· 2 shared T. Mandrup-Poulsen· 2 shared

Activity by Year

2020-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 38 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

4 shared papersImmunology

H. Bielefeldt-Ohmann

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

Targeting host sialic acids in the upper respiratory tract with a broadly-acting neuraminidase to inhibit influenza virus transmission

M. B. Ortigoza, C. L. Mobini, H. L. Rocha, S. Bartlett, C. A. Loomis, J. N. Weiser

This study demonstrates that blocking both 2,3- and 2,6-sialic acid receptors in infant mice using a broadly-acting neuraminidase inhibits influenza virus transmission.

bioRxiv · Jun 2, 2023 · PreprintMicrobiology

Oxysterols drive inflammation via GPR183 during influenza virus and SARS-CoV-2 infection

C. X. Foo, S. Bartlett, K. Y. Chew, M. D. Ngo, H. Bielefeldt-Ohmann, B. J. Arachchige, B. Matthews, S. Reed, R. Wang, M. J. Sweet, L. Burr, J. E. Sinclair, R. Parry, A. Khromykh, K. R. Short, , K. Ronacher

This study identifies oxysterols and GPR183 as drivers of inflammation in the lung during influenza and SARS-CoV-2 infections, showing that targeting GPR183 reduces inflammation and disease severity.

bioRxiv · Jun 14, 2022Immunology

A blunted GPR183/oxysterol axis during dysglycemia results in delayed recruitment of macrophages to the lung during M. tuberculosis infection

M. D. Ngo, S. Bartlett, H. Bielefeldt-Ohmann, C. X. Foo, R. Sinha, B. J. Arachchige, S. J. Reed, T. Mandrup-Poulsen, M. M. Rosenkilde, K. Ronacher

This study shows that dysglycemia impairs the GPR183/oxysterol axis, leading to delayed macrophage recruitment and worsened tuberculosis outcomes in mice.

bioRxiv · Jan 5, 2022Immunology

Pre-diabetes increases tuberculosis disease severity, while high body fat without impaired glucose tolerance is protective

R. Sinha, M. D. Ngo, S. Bartlett, H. Bielefeldt-Ohmann, S. Keshvari, S. Z. Hasnain, M. L. Donovan, J. C. Kling, A. Blumenthal, C. Chen, K. Short, K. Ronacher

bioRxiv · Apr 6, 2021Immunology

GPR183 regulates interferons and bacterial growth during Mycobacterium tuberculosis infection: interaction with type 2 diabetes and TB disease severity

S. Bartlett, A. T. Gemiarto, M. D. Ngo, H. Sajiir, S. Hailu, R. Sinha, C. X. Foo, L. Kleynhans, H. Tshivhula, T. Webber, H. Bielefeldt-Ohmann, N. P. West, A. M. Hiemstra, C. E. MacDonald, L. von Voss Christensen, , K. Ronacher

bioRxiv · Jul 15, 2020Microbiology