Fibroblasts and Osteoblasts in Inflammation and Bone Damage

• Published in: Advances in experimental medicine and biology Vol. 1060; p. 37
• Main Authors: Turner, Jason D, Naylor, Amy J, Buckley, Christopher, Filer, Andrew, Tak, Paul-Peter
• Format: Journal Article
• Language: English
• Published: United States 01.01.2018
• Subjects: Animals; Bone and Bones - pathology; Fibroblasts - pathology; Humans; Inflammation - pathology; Osteoblasts - pathology; Stromal Cells - pathology; Epigenetics; Osteoblast; Stromal immunology; Synovial fibroblast; Fibroblast; Rheumatoid arthritis
• ISSN: 0065-2598
• DOI: 10.1007/978-3-319-78127-3_3

This review discusses the important role fibroblasts play in the process of inflammation and the evidence that these cells may drive the persistence of inflammation. Fibroblasts are key components of the stroma normally involved in maintenance of extracellular matrix and tissue function; however, the term 'fibroblast' is used to describe a heterogeneous population of cells that vary in phenotype both between and within anatomical sites. Fibroblasts possess Toll-like receptors allowing them to respond to pathogen and damage-related signals by producing proinflammatory mediators such as IL-6, PGE , and GM-CSF and can produce a range of chemokines such as CXCL12, CXCL13, and CXCL8 which attract B and T lymphocytes, monocytes, and neutrophils to sites of inflammation. Interactions between leukocytes and fibroblasts can facilitate increased survival of the leukocytes and modulate phenotypes leading to differential gene expression in the presence of mediators involved in inflammation. Fibroblasts also contribute to collateral tissue damage during inflammation through the production of members of the metalloproteinase family and cathepsins and also through induction of osteoclastogenesis leading to increased bone resorption rates. In persistent diseases, fibroblasts obtain an imprinted, aggressive phenotype leading to the production of higher basal levels of proinflammatory cytokines and the ability to damage tissue in the absence of continual stimuli. This aggressive phenotype offers an attractive new target for therapeutics that could help alleviate the burden of persistent inflammation.