scholarly journals IL-10 Could Play a Role in the Interrelation between Diabetes Mellitus and Osteoarthritis

2019 ◽  
Vol 20 (3) ◽  
pp. 768 ◽  
Author(s):  
Sandeep Silawal ◽  
Maximilian Willauschus ◽  
Gundula Schulze-Tanzil ◽  
Clemens Gögele ◽  
Markus Geßlein ◽  
...  

The association between osteoarthritis (OA), obesity and metabolic syndrome suggests an interrelation between OA and diabetes mellitus (DM). Little is known about the role of anti-inflammatory cytokine interleukin (IL)-10 in the interrelation between OA and DM. Hence, the effects of IL-10 under hyperglycemia (HG) and hyperinsulinemia (HI) in human articular chondrocytes (hAC) and chondrosarcoma cell line Okayama University Medical School (OUMS)-27 were examined. HAC and OUMS-27, cultured in normoglycemic (NG) and HG conditions were stimulated with insulin and/or IL-10. Cell survival, metabolic activity, proliferation and extracellular matrix (ECM) synthesis were immunocytochemically examined. No significant differences in vitality of hAC neither in pure NG (NGw/o) nor HG (HGw/o) conditions were found. Applying HI and/or IL-10 in both conditions reduced significantly the vitality of hAC but not of OUMS-27. HG impaired significantly hAC metabolism. When combined with HI + IL-10 or IL-10 alone it decreased also significantly hAC proliferation compared to NGw/o. In OUMS-27 it induced only a trend of impaired proliferation compared to NGw/o. hAC but not OUMS-27 reduced significantly their collagen type (col) I, SOX9 and proteoglycan (PG) synthesis in HG combined with HI +/− IL-10 compared to NGw/o. IL-10 could not moderate HI and HG effects. In contrast to hAC OUMS-27 showed limited sensitivity as DM model.

2021 ◽  
pp. 123-129
Author(s):  
Natasha Shah ◽  
David H. Kruchko ◽  
Eli D. Ehrenpreis

2013 ◽  
Vol 9 (6) ◽  
pp. 894-900 ◽  
Author(s):  
Antonio E. Pontiroli ◽  
Morabito Alberto ◽  
Michele Paganelli ◽  
Alessandro Saibene ◽  
Luca Busetto

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Mamoru Niikura ◽  
Shin-Ichi Inoue ◽  
Fumie Kobayashi

Interleukin- (IL-) 10, anti-inflammatory cytokine, is known to inhibit the protective immune responses against malaria parasites and to be involved in exacerbating parasitemia duringPlasmodiuminfection. In contrast, IL-10 is regarded as necessary for suppressing severe pathology duringPlasmodiuminfection. Here, we summarize the role of IL-10 during murine malaria infection, focusing especially on coinfection with lethal and nonlethal strains of malaria parasites. Recent studies have demonstrated that the major sources of IL-10 are subpopulations of CD4+T cells in humans and mice infected withPlasmodium. We also discuss the influence of innate immunity on the induction of CD4+T cells during murine malaria coinfection.


2017 ◽  
Vol 10 (3) ◽  
Author(s):  
Erick Alexánderson Rosas ◽  
Jonathan Badin Castro ◽  
Diego Adrián Vences Anaya ◽  
Juan José del Moral Díez ◽  
Jessy Steve Masso Bueso ◽  
...  

2020 ◽  
Author(s):  
Tao Chen ◽  
Lixin Fu ◽  
Qiaomei Sun ◽  
Peimei Zhou ◽  
Zai-pei Guo

Abstract Background: IL-35 is a newly anti-inflammatory cytokine which belong to the IL-12 family. Mast cells, as one of the major effector cells in the immune response system, play important roles in the pathogenesis of chronic spontaneous urticarial (CSU). The aim of our study is to explore the inhibited role of IL-35 in HMC-1. Methods: The effects of IL-35 on cell proliferation, cytokine expression and histamine release in human mast cell line (HMC­1) were investigated by CCK8, ELISA or RT-PCR. The phosphorylation of ERK1/2, p38 and JNK1/2, in PMA and A23187 induced HMC-1 cells were detected by Western Blot.Results: We found that IL-35 significantly inhibited the proliferation of HMC-1 cells stimulated by PMA and A23187. IL-35 also down-regulates the released of histamine and the mRNA expression of IL-6 and IL-17 in activated HMC-1. Furthermore, IL-35 markedly inhibited the phosphorylation of ERK1/2, p38 and JNK1/2, in PMA and A23187 induced HMC-1 cells. Conclusions: This study provides first observations on the inhibitory and anti-inflammtory effect of IL-35 on activated HMC-1 cells. We suggest that IL35 may play an inhibited role in the pathogenesis of CSU.


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