IL-6 and IL-10 mRNA were expressed by nine and seven patients respectively in the endometriosis group compared with three and one patients in the control group; this difference was significant (P < 0.05).
IL-10 promoter polymorphisms were associated with the production of anti-CA II ab in patients with endometriosis, suggesting a role in the genetic susceptibility for endometriosis.
IL-10 promoter polymorphisms were associated with the production of anti-CA II ab in patients with endometriosis, suggesting a role in the genetic susceptibility for endometriosis.
Consistent with these data, enzyme-linked immunosorbent assay showed that moderate to severe endometriosis was associated with markedly elevated levels of IL-10 in the peritoneal fluid.
Consistent with these data, enzyme-linked immunosorbent assay showed that moderate to severe endometriosis was associated with markedly elevated levels of IL-10 in the peritoneal fluid.
There were no significant differences in the genotype and allele frequencies of IL-10 gene promoter polymorphisms at position -1082 between the endometriosis and the control groups.
Increased frequency of -819 or -592 C allele and increased protein production of IL-10 in PF in patients with endometriosis compared with controls and correlations of polymorphisms at -819 and -592 sites with protein levels of IL-10 in PF in patients with endometriosis may suggest that polymorphisms at -819 and -592 sites and their protein production are associated with endometriosis risk.
In contrast, the percentages of CD14+ cells producing TNF-alpha, IL-6, IL-10, MCP-1, and IL-8 were significantly higher in PB than PF of women with endometriosis.
Interleukin-10 attenuates TNF-alpha-induced IL-6 synthesis via NF-kappaB and MAPK pathways in endometriotic cells.. Interleukin-10 may play a significant role in the pathogenesis of endometriosis.
Case-control study to investigate the association between endometriosis and four inflammation-related genes: interleukin (IL)-6, IL-10, IL-1 beta, and cyclooxygenase-2.
The aim of this study is to investigate the effect of clarithromycin, one of the major macrolides, and telithromycin, one of the antibiotics belonging to a macrolide group (ketolide), on IL6, IL10 and Ccl2 expression in a rat endometriosis model induced by the surgical transplantation of endometrium onto the peritoneum in 8-week-old female Sprague-Dawley rats.
No significant difference was observed in genotypic or allelic frequencies between control and endometriosis groups for rs498679 (TLR4 gene), rs1799964 (TNF-α gene), rs3024496 (IL-10 gene), neither when comparing endometriosis subgroups (I-II versus III-IV).
Exposure with anti-IL-10 receptor β neutralizing antibody (αhIL-10Rβ) or αTGF-β could partly reverse these effects of ESCs and macrophages on NK cells <i>in vitro</i> These results suggest that the interaction between macrophages and ESCs downregulates cytotoxicity of NK cells possibly by stimulating the secretion of IL-10 and TGF-β, and may further trigger the immune escape of ectopic fragments and promote the occurrence and the development of EMS.
Furthermore, IL-2 concentration was significantly higher in peritoneal fluid (PF) in the endometriosis group (p = .0034), IL-10 concentrations in PF were significantly lower in the early-stages of endometriosis than in the more advanced groups (p = .0439), and IL-4 concentration in PF was significantly higher in more advanced endometriosis (p = .0228).
In endometriosis, TGF-β could affect differentiation of T helper (Th) cells, hence produce more IL-17 and IL-10 to PF and might have an indirect influence on inflammation, which is associated with higher IL-1β and IL-6 levels.
M-MDSCs from EM PBMCs inhibited proliferation and activity in autologous T cells. rhCCL25 promoted IL-10 and GM-CSF secretion and arginase enzymatic activity in CD33<sup>+</sup> CD14<sup>+</sup> CD11b<sup>+</sup> HLA-DR<sup>-</sup> M-MDSCs.
Compared to endometriosis group, IFNγ, IL-7, and IL-15 were observed to be significantly higher in the PF of the control group, and IL-10 was lower in the control group (p < 0.05).