IL-6 secretion in osteoarthritis patients is mediated by chondrocyte-synovial fibroblast cross-talk and is enhanced by obesity

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IL-6 secretion in osteoarthritis patients is mediated by chondrocyte-synovial fibroblast cross-talk and is enhanced by obesity. / Pearson, Mark; Herndler-Brandstetter, Dietmar; Tariq, Mohammad; Nicholson, Thomas; Philp, Ashleigh M.; Smith, Hannah L.; Davis, Edward; Jones, Simon; Lord, Janet.

In: Scientific Reports, Vol. 7, 3451, 14.06.2017.

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Pearson, Mark ; Herndler-Brandstetter, Dietmar ; Tariq, Mohammad ; Nicholson, Thomas ; Philp, Ashleigh M. ; Smith, Hannah L. ; Davis, Edward ; Jones, Simon ; Lord, Janet. / IL-6 secretion in osteoarthritis patients is mediated by chondrocyte-synovial fibroblast cross-talk and is enhanced by obesity. In: Scientific Reports. 2017 ; Vol. 7.

Bibtex

@article{893aab73bd174c3ca50c91a3cedcc125,
title = "IL-6 secretion in osteoarthritis patients is mediated by chondrocyte-synovial fibroblast cross-talk and is enhanced by obesity",
abstract = "Increasing evidence suggests that inflammation plays a central role in driving jointpathology in certain patients with osteoarthritis (OA). Since many patients with OAare obese and increased adiposity is associated with chronic inflammation, weinvestigated whether obese patients with hip OA exhibited differential proinflammatorycytokine signalling and peripheral and local lymphocyte populations,compared to normal weight hip OA patients.No differences in either peripheral blood or local lymphocyte populations were foundbetween obese and normal-weight hip OA patients. However, synovial fibroblastsfrom obese OA patients were found to secrete greater amounts of the proinflammatorycytokine IL-6, compared to those from normal-weight patients (p<0.05),which reflected the greater levels of IL-6 detected in the synovial fluid of the obeseOA patients. Investigation into the inflammatory mechanism demonstrated that IL-6secretion from synovial fibroblasts was induced by chondrocyte-derived IL-6.Furthermore, this IL-6 inflammatory response, mediated by chondrocyte-synovialfibroblast cross-talk, was enhanced by the obesity-related adipokine leptin. Thisstudy suggests that obesity enhances the cross-talk between chondrocytes andsynovial fibroblasts via raised levels of the pro-inflammatory adipokine leptin, leadingto greater production of IL-6 in OA patients.",
keywords = "IL-6 , chondrocytes , fibroblasts, obesity , synovial inflammation , leptin",
author = "Mark Pearson and Dietmar Herndler-Brandstetter and Mohammad Tariq and Thomas Nicholson and Philp, {Ashleigh M.} and Smith, {Hannah L.} and Edward Davis and Simon Jones and Janet Lord",
year = "2017",
month = jun,
day = "14",
doi = "10.1038/s41598-017-03759-w",
language = "English",
volume = "7",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",

}

RIS

TY - JOUR

T1 - IL-6 secretion in osteoarthritis patients is mediated by chondrocyte-synovial fibroblast cross-talk and is enhanced by obesity

AU - Pearson, Mark

AU - Herndler-Brandstetter, Dietmar

AU - Tariq, Mohammad

AU - Nicholson, Thomas

AU - Philp, Ashleigh M.

AU - Smith, Hannah L.

AU - Davis, Edward

AU - Jones, Simon

AU - Lord, Janet

PY - 2017/6/14

Y1 - 2017/6/14

N2 - Increasing evidence suggests that inflammation plays a central role in driving jointpathology in certain patients with osteoarthritis (OA). Since many patients with OAare obese and increased adiposity is associated with chronic inflammation, weinvestigated whether obese patients with hip OA exhibited differential proinflammatorycytokine signalling and peripheral and local lymphocyte populations,compared to normal weight hip OA patients.No differences in either peripheral blood or local lymphocyte populations were foundbetween obese and normal-weight hip OA patients. However, synovial fibroblastsfrom obese OA patients were found to secrete greater amounts of the proinflammatorycytokine IL-6, compared to those from normal-weight patients (p<0.05),which reflected the greater levels of IL-6 detected in the synovial fluid of the obeseOA patients. Investigation into the inflammatory mechanism demonstrated that IL-6secretion from synovial fibroblasts was induced by chondrocyte-derived IL-6.Furthermore, this IL-6 inflammatory response, mediated by chondrocyte-synovialfibroblast cross-talk, was enhanced by the obesity-related adipokine leptin. Thisstudy suggests that obesity enhances the cross-talk between chondrocytes andsynovial fibroblasts via raised levels of the pro-inflammatory adipokine leptin, leadingto greater production of IL-6 in OA patients.

AB - Increasing evidence suggests that inflammation plays a central role in driving jointpathology in certain patients with osteoarthritis (OA). Since many patients with OAare obese and increased adiposity is associated with chronic inflammation, weinvestigated whether obese patients with hip OA exhibited differential proinflammatorycytokine signalling and peripheral and local lymphocyte populations,compared to normal weight hip OA patients.No differences in either peripheral blood or local lymphocyte populations were foundbetween obese and normal-weight hip OA patients. However, synovial fibroblastsfrom obese OA patients were found to secrete greater amounts of the proinflammatorycytokine IL-6, compared to those from normal-weight patients (p<0.05),which reflected the greater levels of IL-6 detected in the synovial fluid of the obeseOA patients. Investigation into the inflammatory mechanism demonstrated that IL-6secretion from synovial fibroblasts was induced by chondrocyte-derived IL-6.Furthermore, this IL-6 inflammatory response, mediated by chondrocyte-synovialfibroblast cross-talk, was enhanced by the obesity-related adipokine leptin. Thisstudy suggests that obesity enhances the cross-talk between chondrocytes andsynovial fibroblasts via raised levels of the pro-inflammatory adipokine leptin, leadingto greater production of IL-6 in OA patients.

KW - IL-6

KW - chondrocytes

KW - fibroblasts

KW - obesity

KW - synovial inflammation

KW - leptin

U2 - 10.1038/s41598-017-03759-w

DO - 10.1038/s41598-017-03759-w

M3 - Article

C2 - 28615667

VL - 7

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

M1 - 3451

ER -