English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background  Macrophages play prominent roles in bacteria recognition and clearance, including  Borrelia burgdorferi  ( Bb ), the Lyme disease spirochete. To elucidate mechanisms by which MyD88/TLR signaling enhances clearance of  Bb  by macrophages, we studied wildtype (WT) and MyD88 −/−   Bb -stimulated bone marrow-derived macrophages (BMDMs).    Results  MyD88 −/−  BMDMs exhibit impaired uptake of spirochetes but comparable maturation of phagosomes following internalization of spirochetes. RNA-sequencing of infected WT and MyD88 −/−  BMDMs identified a large cohort of differentially expressed MyD88-dependent genes associated with re-organization of actin and cytoskeleton during phagocytosis along with several MyD88-independent chemokines involved in inflammatory cell recruitment. We computationally generated networks which identified several MyD88-dependent intermediate proteins ( Rhoq  and  Cyfip1 ) that are known to mediate inflammation and phagocytosis respectively.    Conclusion  Our findings show that MyD88 signaling enhances, but is not required, for bacterial uptake or phagosomal maturation and provide mechanistic insights into how MyD88-mediated phagosomal signaling enhances  Bb  uptake and clearance.    Supplementary Information  The online version contains supplementary material available at 10.1186/s12865-021-00418-8.

bmc immunology

Macrophage mediated recognition and clearance of Borrelia burgdorferi elicits MyD88-dependent and -independent phagosomal signals that contribute to phagocytosis and inflammation