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19.03.2020 | Original Research Paper | Ausgabe 5/2020

Inflammation Research 5/2020

IL-18/IL-18R1 promotes circulating fibrocyte differentiation in the aging population

Zeitschrift:
Inflammation Research > Ausgabe 5/2020
Autoren:
Xiao-Hui Niu, Yun-Peng Xie, Song Yang, Yanchun Chen, Liang Xu, Ying Zhang, Yang Liu
Wichtige Hinweise
Communicated by John Di Battista.

Electronic supplementary material

The online version of this article (https://​doi.​org/​10.​1007/​s00011-020-01330-4) contains supplementary material, which is available to authorized users.
Xiao-Hui Niu and Yun-Peng Xie contributed equally to this work.

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Abstract

Background

Fibrosis in multiple organs increases with age. Circulating fibrocytes are bone-marrow-derived mesenchymal progenitors that contribute to heart, lung, and kidney fibrosis under the diseased conditions. Whether circulating fibrocytes contribute to aging-related fibrosis is very limited.

Methods and results

We measured the proportion and differentiation of circulating fibrocytes (CD45+/CD34+/collagen I+) from elders (n = 12) and adults (n = 12) using flow cytometry. Differentiated fibrocytes in the culture dishes were isolated and microarray was performed. The percentage of circulating fibrocytes in elders (1.95 ± 0.43%) was comparable to that in the adults (1.71 ± 0.38%). Cultured fibrocytes displayed enhanced potential of differentiation in the elder group (67.91 ± 5.88%) vs the adult group (44.03 ± 7.98%). In addition, expression of fibroblast activation markers and cell migratory ability were also increased in differentiated fibrocytes from elders. Microarray analysis revealed that differentiated fibrocytes from elders expressed high level of interleukin-18 (IL-18) receptor 1 (IL-18R1). Furthermore, we found IL-18 was elevated in the plasma of elders and IL-18/IL-18R1 was shown to promote fibrocyte differentiation.

Conclusion

Circulating fibrocytes from elders had an enhanced capacity to differentiate into myofibroblasts, and might contribute to age-dependent fibrosis. Age-dependent increment of differentiation at least in part arose from their enhanced expression of IL-18R1. Inhibiting fibrocyte differentiation might be useful as an adjuvant treatment to delay the fibrosis process in aging population.

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