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Biology subjects

Spitzer, G.

Publications and source records attributed to Spitzer, G..

2 recordsLinked to original sources

Allergy-induced systemic inflammation impairs tendon quality

Treatment of tendinopathies still present a major challenge, since the aetiology of the disease remains poorly understood. To determine whether the systemic inflammation accompanying predisposing factors including rheumatoid arthritis, diabetes or smoking contributes to the onset of tendinopathy, we studied the effect of a systemic inflammation induced by an allergic episode on tendon properties. To this end, we elicited an allergic response in mice by exposing them to a plant allergen and subsequently analysed both their flexor and Achilles tendons. Biomechanical testing and histological analysis revealed that tendons from allergic mice not only showed a significant reduction of both elastic modulus and tensile stress, but also alterations of the tendon matrix. Moreover, 3D tendon-like constructs treated with sera from allergic mice displayed a matrix-remodelling expression profile and the expression of macrophage-associated markers and matrix metalloproteinase 2 (MMP2) was increased in allergic Achilles tendons. Analysing data from an epidemiologic study comprising data from more than 10.000 persons, we found that persons suffering from an allergic condition appeared to have an increased propensity to develop a tendinopathy. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=137 SRC="FIGDIR/small/450910v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@1263836org.highwire.dtl.DTLVardef@349621org.highwire.dtl.DTLVardef@6c9142org.highwire.dtl.DTLVardef@1b49bdd_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗

CX3CL1 and CX3CR1 Expressing Tendon Cells - A novel Immune Cell Population in the Tendon Core

Tendon disorders frequently occur and recent evidence has clearly implicated the presence of immune cells and inflammatory events during early tendinopathy. However, the origin and properties of these cells remain poorly defined. Therefore, the aim of this study was to determine the presence of myleoid cells in healthy rodent and human tendon tissue and to characterize them. Using various transgenic reporter mouse models, we demonstrate the presence of tendon cells in the dense matrix of the tendon core expressing the fractalkine (Fkn) receptor CX3CR1 and its cognate ligand CX3CL1/Fkn. Pro-inflammatory stimulation of 3D tendon-like constructs in vitro resulted in a significant increase in the expression of IL-1{beta}, IL-6, Mmp3, Mmp9, Cx3cl1, and epiregulin which has been reported to contribute to inflammation, wound healing, and tissue repair. Furthermore, we demonstrate that inhibition of the fractalkine receptor blocked tendon cell migration in vitro and show the presence of CX3CR1/CX3CL1/EREG expressing cells in healthy human tendons. Taken together, we demonstrate the presence of CX3CL1+/CX3CR1+ \"tenophages\" within the healthy tendon proper potentially fulfilling surveillance functions in tendons.\n\nSummary StatementHere, we demonstrate the presence of a macrophage-like, CX3CL1/CX3CR1-expressing cell population within the healthy tendon proper potentially fulfilling a surveillance function.

cell biology↗