Search results for " Ankylosing spondylitis"
showing 8 items of 8 documents
AUTOPHAGY, BUT NOT THE UNFOLDED PROTEIN RESPONSE, REGULATES THE EXPRESSION OF IL-23 IN THEGUT OF PATIENTS WITH ANKYLOSING SPONDYLITIS AND SUBCLINICAL…
2013
Background: IL-23 is a heterodimeric cytokine that has been implicated in the pathogenesis of Ankylosing Spondylitis (AS). High serum and tissue levels for this cytokine have been demonstrated in AS and correlated with entheseal inflammation but the mechanisms responsible for its over-expression are currently not clear. Objectives: The aim of the study was to clarify the immunological mechanisms underlying the increased IL-23 expression in the gut of AS patients. Methods: Consecutive gut biopsies from 20 HLA-B27+ AS patients and 10 normal subjects were considered for the present study. The occurrence of HLA-B27 misfolding was studied by assessing the co-localization of HLA-B heavy chains (H…
Association of interleukin-10G microsatellite polymorphism with the susceptibility of ankylosing spondylitis
2013
Study suggests an association of IL10.G poly- morphisms with AS which might contribute to the increased or decreased susceptibility to AS. IL10.G8 and G7 microsatellites alleles appear as protective alleles against the development of AS in the German subjects investigated here. Allele IL10.G9 seems to be a risk factor for the development of AS. This protective effect of variant promoter alleles could be related to differences in IL- 10 production, which may be clinically relevant.
Response to: 'IL-23 expression and activation of autophagy in synovium and PBMCs of HLA-B27 positive patients with ankylosing spondylitis' by Neerinc…
2014
We read with interest the study by Neerinckx et al 1 addressing the expression of interleukin (IL)-23p19 and of autophagy genes in the synovium and in the peripheral blood mononuclear cells of patients with ankylosing spondylitis (AS). Differently from our observation in the gut,2 the authors failed to demonstrate any significant increase by RT-PCR in the expression of synovium autophagy-related genes (ATG16L1, IRGM, MAP1LC3A, ATG5, HSPA8 and HSP90AA1) together with no significant overexpression of IL-23p19 compared with disease and healthy controls. We have previously demonstrated by immunohistochemistry that in the …
Macrophage phenotype in the subclinical gut inflammation of patients with ankylosing spondylitis
2014
OBJECTIVE: Long-term evolution of subclinical gut inflammation to overt Crohn's disease (CD) has been described in AS patients. The aim of this study was to evaluate macrophage polarization occurring in the inflamed gut of patients with AS. METHODS: Twenty-seven HLA-B27(+) AS patients, 20 CD patients and 17 normal controls were consecutively enrolled. Classic M1 (iNOS(+)IL-10(-)), resolution phase (iNOS(+)IL-10(+)), M2 and CD14(+) macrophages were characterized by immunohistochemistry and flow cytometry. Quantitative gene expression analysis of IFN-γ, IL-4, IL-5, IL-33 and STAT6 was performed by real time PCR. RESULTS: Classic M1 macrophages were expanded in CD and AS, where resolution phas…
Disease-associated polymorphisms in ERAP1 do not alter endoplasmic reticulum stress in patients with ankylosing spondylitis
2014
The mechanism by which human leukocyte antigen B27 (HLA-B27) contributes to ankylosing spondylitis (AS) remains unclear. Genetic studies demonstrate that association with and interaction between polymorphisms of endoplasmic reticulum aminopeptidase 1 (ERAP1) and HLA-B27 influence the risk of AS. It has been hypothesised that ERAP1-mediated HLA-B27 misfolding increases endoplasmic reticulum (ER) stress, driving an interleukin (IL) 23-dependent, pro-inflammatory immune response. We tested the hypothesis that AS-risk ERAP1 variants increase ER-stress and concomitant pro-inflammatory cytokine production in HLA-B27(+) but not HLA-B27(-) AS patients or controls. Forty-nine AS cases and 22 healthy…
Overexpression of interleukin-23, but not interleukin-17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis
2009
Objective Subclinical gut inflammation is common in spondylarthritis, but the immunologic abnormalities underlying this process are undefined. Perturbation of the interleukin-23 (IL-23)/Th17 axis has emerged as a fundamental trigger of chronic inflammation. This study was undertaken to investigate the expression and tissue distribution of IL-23/Th17–related molecules in Crohn's disease (CD) and in subclinical gut inflammation in ankylosing spondylitis (AS). Methods Quantitative gene expression analysis of Th1/Th2 and IL-23/Th17 responses was performed in intestinal biopsy samples obtained from 12 patients with CD, 15 patients with AS, and 13 controls. IL-23 tissue distribution and identific…
Over-expression of paneth cell-derived anti-microbial peptides in the gut of patients with ankylosing spondylitis and subclinical intestinal inflamma…
2010
OBJECTIVES: Subclinical gut inflammation has been demonstrated in patients with AS. Altered expression of paneth cell (PC) anti-microbial peptides have been reported in the inflamed ileum of patients with Crohn's disease (CD). Here, we investigated the expression of PC-derived peptides in subclinical gut inflammation in AS. METHODS: Multiple adjacent mucosal biopsies from terminal ileum were obtained from 25 patients with AS, 30 CD and 15 healthy controls (HCs). Expression of human α-defensin 5 (HD-5), phospholipase A2 (PLA2), lysozyme and SOX-9 molecules was assessed by quantitative Taqman RT-PCR on mucosal samples. Immunohistochemistry with anti-human HD-5 antibody and genotyping of relev…
Increased expression of interleukin-32 in the inflamed ileum of ankylosing spondylitis patients
2012
Objective. To study the mRNA expression and protein tissue distribution of IL-32 in ileal biopsy specimens from patients with AS. Methods. Quantitative gene expression analysis, by real-time PCR, of IL-32, IL-1b, IL-10, TNF-a and IFN-g was performed on ileal biopsies of 15 AS and 15 Crohn’s disease (CD) patients and 10 healthy subjects (HSs). IL-32 tissue distribution was evaluated by immunohistochemistry. The effect of IL-32 on the production of IL-10 by intestinal epithelial cell lines was also evaluated. Results. In the ileal specimens of patients with AS and intestinal chronic inflammation, significant up-regulation of IL-32 at both the mRNA and protein levels was found as compared with…