Fibroblasts and Osteoblasts in Inflammation and Bone Damage

Research output: Chapter in Book/Report/Conference proceedingChapter

Standard

Fibroblasts and Osteoblasts in Inflammation and Bone Damage. / Turner, Jason D.; Naylor, Amy J.; Buckley, Christopher; Filer, Andrew; Tak, Paul-Peter.

Stromal Immunology. ed. / Benjamin M. J. Owens; Matthew A. Lakins. Vol. 1060 Springer, 2018. p. 37-54 (Advances in Experimental Medicine and Biology).

Research output: Chapter in Book/Report/Conference proceedingChapter

Harvard

Turner, JD, Naylor, AJ, Buckley, C, Filer, A & Tak, P-P 2018, Fibroblasts and Osteoblasts in Inflammation and Bone Damage. in BMJ Owens & MA Lakins (eds), Stromal Immunology. vol. 1060, Advances in Experimental Medicine and Biology, Springer, pp. 37-54. https://doi.org/10.1007/978-3-319-78127-3_3

APA

Turner, J. D., Naylor, A. J., Buckley, C., Filer, A., & Tak, P-P. (2018). Fibroblasts and Osteoblasts in Inflammation and Bone Damage. In B. M. J. Owens, & M. A. Lakins (Eds.), Stromal Immunology (Vol. 1060, pp. 37-54). (Advances in Experimental Medicine and Biology). Springer. https://doi.org/10.1007/978-3-319-78127-3_3

Vancouver

Turner JD, Naylor AJ, Buckley C, Filer A, Tak P-P. Fibroblasts and Osteoblasts in Inflammation and Bone Damage. In Owens BMJ, Lakins MA, editors, Stromal Immunology. Vol. 1060. Springer. 2018. p. 37-54. (Advances in Experimental Medicine and Biology). https://doi.org/10.1007/978-3-319-78127-3_3

Author

Turner, Jason D. ; Naylor, Amy J. ; Buckley, Christopher ; Filer, Andrew ; Tak, Paul-Peter. / Fibroblasts and Osteoblasts in Inflammation and Bone Damage. Stromal Immunology. editor / Benjamin M. J. Owens ; Matthew A. Lakins. Vol. 1060 Springer, 2018. pp. 37-54 (Advances in Experimental Medicine and Biology).

Bibtex

@inbook{6e5ba6515f8745c7b942be81f907e0e5,
title = "Fibroblasts and Osteoblasts in Inflammation and Bone Damage",
abstract = "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, PGE2, 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.",
keywords = "fibroblast, synovial fibroblast, osteoblast, rheumatoid arthritis, stromal immunology, epigenetics",
author = "Turner, {Jason D.} and Naylor, {Amy J.} and Christopher Buckley and Andrew Filer and Paul-Peter Tak",
year = "2018",
month = "8",
day = "29",
doi = "10.1007/978-3-319-78127-3_3",
language = "English",
isbn = "978-3-319-78125-9",
volume = "1060",
series = "Advances in Experimental Medicine and Biology",
publisher = "Springer",
pages = "37--54",
editor = "Owens, {Benjamin M. J.} and Lakins, {Matthew A.}",
booktitle = "Stromal Immunology",

}

RIS

TY - CHAP

T1 - Fibroblasts and Osteoblasts in Inflammation and Bone Damage

AU - Turner, Jason D.

AU - Naylor, Amy J.

AU - Buckley, Christopher

AU - Filer, Andrew

AU - Tak, Paul-Peter

PY - 2018/8/29

Y1 - 2018/8/29

N2 - 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, PGE2, 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.

AB - 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, PGE2, 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.

KW - fibroblast

KW - synovial fibroblast

KW - osteoblast

KW - rheumatoid arthritis

KW - stromal immunology

KW - epigenetics

U2 - 10.1007/978-3-319-78127-3_3

DO - 10.1007/978-3-319-78127-3_3

M3 - Chapter

C2 - 30155621

SN - 978-3-319-78125-9

VL - 1060

T3 - Advances in Experimental Medicine and Biology

SP - 37

EP - 54

BT - Stromal Immunology

A2 - Owens, Benjamin M. J.

A2 - Lakins, Matthew A.

PB - Springer

ER -