Toll-like Receptors Induce a Phagocytic Gene Program through p38
Citations Over TimeTop 10% of 2003 papers
Abstract
Toll-like receptor (TLR) signaling and phagocytosis are hallmarks of macrophage-mediated innate immune responses to bacterial infection. However, the relationship between these two processes is not well established. Our data indicate that TLR ligands specifically promote bacterial phagocytosis, in both murine and human cells, through induction of a phagocytic gene program. Importantly, TLR-induced phagocytosis of bacteria was found to be reliant on myeloid differentiation factor 88-dependent signaling through interleukin-1 receptor-associated kinase-4 and p38 leading to the up-regulation of scavenger receptors. Interestingly, individual TLRs promote phagocytosis to varying degrees with TLR9 being the strongest and TLR3 being the weakest inducer of this process. We also demonstrate that TLR ligands not only amplify the percentage of phagocytes uptaking Escherichia coli, but also increase the number of bacteria phagocytosed by individual macrophages. Taken together, our data describe an evolutionarily conserved mechanism by which TLRs can specifically promote phagocytic clearance of bacteria during infection.
Related Papers
- → Bacterial Lipopolysaccharide and IFN-γ Induce Toll-Like Receptor 2 and Toll-Like Receptor 4 Expression in Human Endothelial Cells: Role of NF-κB Activation(2001)448 cited
- → Different effects ofP. gingivalisLPS andE. coliLPS on the expression of interleukin-6 in human gingival fibroblasts(2013)69 cited
- → TLR9-deficiency reduces TLR1, TLR2 and TLR3 expressions in Leishmania major-infected macrophages(2015)12 cited
- Effects of P1 Infection on Transcriptional Levels of TLRs in Peripheral Blood Mononuclear Cells of Piglets(2010)
- → Η TLR-4 και TLR-9 - εξαρτώμενη ανοσιακή απάντηση στο ακανθοκυτταρικό καρκίνωμα γλώσσας(2020)