Author

S. L. Bell

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

Biology Disciplines

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Immunology· 5 Microbiology· 2

Signature Assays, Organisms & Methods

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Research Focus:host-pathogen & immune response· 6 Approach:experimental assay· 5 Organism:mouse· 5 Assay:proteomics· 4 Research Focus:cell type annotation· 2 Research Focus:development & morphogenesis· 2 Approach:genetic perturbation / CRISPR· 2 Organism:human· 2

Frequent Co-Authors

R. O. WatsoniD· 7 shared K. L. PatrickiD· 6 shared K. J. Vail· 3 shared A. P. West· 2 shared C. G. Weindel· 2 shared J. S. Cox· 2 shared P. Li· 2 shared S. Torres-Odio· 2 shared

Activity by Year

2019-2021 · peak 4/yr

Co-Author Collaboration Network

10 top collaborators · 30 mutual co-author links

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7 shared papersImmunology

R. O. WatsonORCID

Mutual co-authors in cluster

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7 papers

Recent·Most cited

Mitochondrial dysfunction promotes alternative gasdermin D-mediated inflammatory cell death and susceptibility to infection

C. G. Weindel, X. Zhao, E. Martinez, S. L. Bell, K. J. Vail, A. K. Coleman, J. J. VanPortfliet, B. Zhao, C. Mabry, P. Li, P. West, J. Karpac, K. L. Patrick, R. O. Watson

This study shows that mitochondrial dysfunction caused by Lrrk2G2019S promotes non-pyroptotic cell death via GSDMD and increases susceptibility to infection.

bioRxiv · Nov 18, 2021 · PreprintImmunology

Galectin-8 senses phagosomal damage and recruits selective autophagy adapter TAX1BP1 to control Mycobacterium tuberculosis infection in macrophages

S. L. Bell, K. L. Lopez, J. S. Cox, K. L. Patrick, R. O. Watson

This study identifies galectin-8 as a sensor for damaged Mtb-containing phagosomes that recruits TAX1BP1 to promote selective autophagy and control Mtb replication in macrophages.

mBio · Aug 31, 2021Peer-reviewedMicrobiology

The opportunistic intracellular bacterial pathogen Rhodococcus equi elicits type I interferons by engaging cytosolic DNA sensing in macrophages

K. J. Vail, B. Petri da Silveira, S. L. Bell, A. I. Bordin, N. D. Cohen, K. L. Patrick, R. O. Watson

This paper shows that Rhodococcus equi triggers type I interferons in macrophages via cytosolic DNA sensing, independent of its virulence plasmid.

bioRxiv · Mar 28, 2021Immunology

Interactions between fungal hyaluronic acid and host CD44 promote internalization by recruiting host autophagy proteins to forming phagosomes

S. Ding, A. Pandey, X. Feng, J. Yang, L. F. da Costa, R. B. Mouneimne, A. Rice-Ficht, S. L. Bell, R. O. Watson, K. L. Patrick, Q.-M. Qin, T. A. Ficht, P. de Figueiredo

This paper shows fungal hyaluronic acid interacts with host CD44 to recruit autophagy proteins to phagosomes, promoting fungal internalization via a Ca2+ -CaMKKβ-AMPK-ULK1 signaling pathway.

iScience · Mar 1, 2021Peer-reviewedMicrobiology

Type I interferon potentiates metabolic dysfunction, inflammation, and accelerated aging in mtDNA mutator mice

Y. Lei, C. G. Martinez, S. Torres-Odio, S. L. Bell, C. E. Birdwell, J. D. Bryant, C. W. Tong, R. O. Watson, L. C. West, A. P. West

This study shows that type I interferon activation worsens metabolic issues, inflammation, and aging in mice with mitochondrial DNA mutations.

bioRxiv · Sep 22, 2020Immunology

TRIM14 is a key regulator of the type I interferon response during Mycobacterium tuberculosis infection

C. T. Hoffpauir, S. L. Bell, K. O. West, T. Jing, S. Torres-Odio, J. S. Cox, A. P. West, P. Li, K. L. Patrick, R. O. Watson

This study identifies TRIM14 as a negative regulator of the type I interferon response in macrophages during Mycobacterium tuberculosis infection, showing it enhances resolution of the response and limits bacterial replication.

The Journal of Immunology · Jul 1, 2020Peer-reviewedImmunology

LRRK2 regulates innate immune responses and neuroinflammation during Mycobacterium tuberculosis infection

C. G. Weindel, S. L. Bell, T. E. Huntington, K. J. Vail, R. Srinivasan, K. L. Patrick, R. O. Watson

This study shows LRRK2 regulates immune responses and neuroinflammation during Mycobacterium tuberculosis infection, linking it to neurodegenerative disease mechanisms.

bioRxiv · Jul 26, 2019Immunology