MyD88-dependent and -independent phagosomal signals in Macrophage mediated recognition and clearance of Borrelia burgdorferi (Lyme disease spirochete)

Lyme disease is a highly prevalent tick-borne illness caused by the spirochetal bacterium Borrelia burgdorferi (Bb). The macrophage is a principal component of the innate immune response and has been observed at sites of Bb infection. Macrophages have the phagocytic and signaling machinery necessary to bind, engulf, and degrade Bb.

Previous studies by our collaborator, The Salazar and Hawley lab, have emphasized that uptake and degradation of Bb by phagocytic cells, including monocytes and macrophages, are critical in eliciting the inflammatory response to the bacterium.

The objective of this collaborations is to study the role of the adaptor protein MyD88 in bacterial uptake and phagosomal signaling in macrophages. With bioinformatics tools and network analysis approaches we are analyzing RNA-seq data of stimulated bone marrow-derived macrophages (BMDMs) with Borrelia burgdorferi (Bb), the causative agent of Lyme disease. We will dissect the different signaling pathways with a particular attention to those involving MyD88, inflammation, actin and cytoskeleton organization.

More information can be found in my collaborator’s Spirochete Research Lab website: https://health.uconn.edu/spirochete-lab/salazar-laboratory/research/

Publications

. Macrophage mediated recognition and clearance of Borrelia burgdorferinelicits MyD88-dependent and -independent phagosomal signals that contribute to phagocytosis and inflammation. https://www.biorxiv.org/content/10.1101/593566v1, 2019.

Preprint Project