Bacterial Cell Wall Constituents Induce Hepcidin Expression in Macrophages Through MyD88 Signaling
| Autor: | Antonio Layoun, Manuela M. Santos |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
Lipopolysaccharides
Lipopolysaccharide Iron Immunology Inflammation Cell Line Proinflammatory cytokine Mice chemistry.chemical_compound Hepcidins Cell Wall Hepcidin hemic and lymphatic diseases medicine Animals Immunology and Allergy Autocrine signalling Mice Knockout Mice Inbred C3H biology Interleukin-6 Macrophages nutritional and metabolic diseases Toll-Like Receptor 2 Culture Media Cell biology Mice Inbred C57BL Toll-Like Receptor 4 TLR2 chemistry Biochemistry Myeloid Differentiation Factor 88 Macrophages Peritoneal TLR4 biology.protein Female Signal transduction medicine.symptom Antimicrobial Cationic Peptides Signal Transduction |
| Zdroj: | Inflammation. 35:1500-1506 |
| ISSN: | 1573-2576 0360-3997 |
| DOI: | 10.1007/s10753-012-9463-4 |
| Popis: | Hepcidin is a key regulator of iron recycling by macrophages that is synthesized mainly by hepatocytes but also by macrophages. However, very little is known about the molecular regulation of hepcidin in macrophages. In the present study, we investigated hepcidin regulation in the RAW264.7 macrophage cell line and in murine peritoneal macrophages stimulated with different Toll-like receptor (TLR) ligands. We found that TLR-2 and TLR-4 ligands activated hepcidin expression in RAW264.7 cells and in wild-type murine peritoneal macrophages, but not in murine peritoneal macrophages isolated from TLR2(-/-), TLR-4-deficient or MyD88(-/-) mice. IL-6 production by RAW264.7 cells stimulated with lipopolysaccharide (LPS, TLR4 ligand) was enhanced by high amounts of iron present in the culture medium. We conclude that hepcidin expression in macrophages is regulated mainly through TLR2 and TLR4 receptors via the MyD88-dependent signaling pathway and that autocrine regulation of iron accumulation in macrophages by hepcidin may affect the levels of proinflammatory cytokine production. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink