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Type I IFN exacerbates disease in tuberculosis-susceptible mice by inducing neutrophil-mediated lung inflammation and NETosis (2020)
Journal Article
Moreira-Teixeira, L., Stimpson, P. J., Stavropoulos, E., Hadebe, S., Chakravarty, P., Ioannou, M., …O’Garra, A. (2020). Type I IFN exacerbates disease in tuberculosis-susceptible mice by inducing neutrophil-mediated lung inflammation and NETosis. Nature Communications, 11(1), 5566. https://doi.org/10.1038/s41467-020-19412-6

Abstract: Tuberculosis (TB) is a leading cause of mortality due to infectious disease, but the factors determining disease progression are unclear. Transcriptional signatures associated with type I IFN signalling and neutrophilic inflammation were sh... Read More about Type I IFN exacerbates disease in tuberculosis-susceptible mice by inducing neutrophil-mediated lung inflammation and NETosis.

Sost haploinsufficiency provokes peracute lethal cardiac tamponade without rescuing the osteopenia in a mouse model of excess glucocorticoids (2019)
Journal Article
Javaheri, B., Herbert, E., Hopkinson, M., Al-Jazzar, A., & Pitsillides, A. A. (2019). Sost haploinsufficiency provokes peracute lethal cardiac tamponade without rescuing the osteopenia in a mouse model of excess glucocorticoids. American Journal of Pathology, 189(4), 753-761. https://doi.org/10.1016/j.ajpath.2018.12.007

Glucocorticoid-induced secondary osteoporosis is the most predictable side-effect of this anti-inflammatory. One of the main mechanisms by which glucocorticoids achieve such deleterious outcome in bone is by antagonizing Wnt/β-catenin signalling. Scl... Read More about Sost haploinsufficiency provokes peracute lethal cardiac tamponade without rescuing the osteopenia in a mouse model of excess glucocorticoids.