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Sci Rep. 2017 Oct 2;7(1):12492. doi: 10.1038/s41598-017-12666-z.

Mast Cell-Intervertebral disc cell interactions regulate inflammation, catabolism and angiogenesis in Discogenic Back Pain.

Author information

1
Department of Biomedical Engineering, The Ohio State University, Columbus Ohio, 201 Davis Heart and Lung Research Institute, 473 W 12th Avenue, Columbus, Ohio, 43210, USA.
2
Department of Orthopedics, The Ohio State University Wexner Medical Center, 1070 OSU CarePoint East, 543 Taylor Avenue, Columbus, Ohio, 43203, USA.
3
Department of Internal Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, The Ohio State University, 201 Davis Heart and Lung Research Institute, 473 West 12th Avenue, Columbus, Ohio, 43210, USA.
4
Division of Cell Matrix Biology and Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Stopford Building, Oxford Road, Manchester, M13 9PT, United Kingdom.
5
NIHR Manchester Musculoskeletal Biomedical Research Centre, Manchester Academic Health Science Centre, Central Manchester NHS Foundation Trust, Manchester, United Kingdom.
6
Department of Biomedical Engineering, The Ohio State University, Columbus Ohio, 201 Davis Heart and Lung Research Institute, 473 W 12th Avenue, Columbus, Ohio, 43210, USA. devina.purmessur@osumc.edu.
7
Department of Orthopedics, The Ohio State University Wexner Medical Center, 1070 OSU CarePoint East, 543 Taylor Avenue, Columbus, Ohio, 43203, USA. devina.purmessur@osumc.edu.

Abstract

Low back pain (LBP) is a widespread debilitating disorder of significant socio-economic importance and intervertebral disc (IVD) degeneration has been implicated in its pathogenesis. Despite its high prevalence the underlying causes of LBP and IVD degeneration are not well understood. Recent work in musculoskeletal degenerative diseases such as osteoarthritis have revealed a critical role for immune cells, specifically mast cells in their pathophysiology, eluding to a potential role for these cells in the pathogenesis of IVD degeneration. This study sought to characterize the presence and role of mast cells within the IVD, specifically, mast cell-IVD cell interactions using immunohistochemistry and 3D in-vitro cell culture methods. Mast cells were upregulated in painful human IVD tissue and induced an inflammatory, catabolic and pro-angiogenic phenotype in bovine nucleus pulposus and cartilage endplate cells at the gene level. Healthy bovine annulus fibrosus cells, however, demonstrated a protective role against key inflammatory (IL-1β and TNFα) and pro-angiogenic (VEGFA) genes expressed by mast cells, and mitigated neo-angiogenesis formation in vitro. In conclusion, mast cells can infiltrate and elicit a degenerate phenotype in IVD cells, enhancing key disease processes that characterize the degenerate IVD, making them a potential therapeutic target for LBP.

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