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Proceedings of the 2016 Childhood Arthritis and Rheumatology Research Alliance (CARRA) Scientific Meeting : Toronto, Canada UC Davis UC Davis Previously Published Works Title Proceedings of the 2016 Childhood Arthritis and Rheumatology Research Alliance (CARRA) Scientific Meeting : Toronto, Canada. 14-17 April 2016. Permalink https://escholarship.org/uc/item/83s8117x Journal Pediatric rheumatology online journal, 14 Suppl 1(S1) ISSN 1546-0096 Authors Fotis, Lampros Shaikh, Nur Baszis, Kevin et al. Publication Date 2016-07-12 DOI 10.1186/s12969-016-0098-0 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Pediatric Rheumatology 2016, Volume 14 Suppl 1 DOI 10.1186/s12969-016-0098-0 MEETINGABSTRACTS Open Access Proceedings of the 2016 Childhood Arthritis and Rheumatology Research Alliance (CARRA) Scientific Meeting Toronto, Canada. 14-17 April 2016 Published: 12 July 2016 P1 P2 Serologic evidence of gut-driven systemic inflammation in juvenile Oral health and anti-citrullinated peptide antibodies (ACPA) in idiopathic arthritis juvenile idiopathic arthritis Lampros Fotis, Nur Shaikh, Kevin Baszis, Anthony French, Phillip Tarr Sriharsha Grevich1, Peggy Lee2, Sarah Ringold3, Brian Leroux4, Washington University School of Medicine, St Louis, Missouri, USA Hannah Leahey5, Megan Yuasa5, Jessica Foster6, Jeremy Sokolove7, Correspondence: Lampros Fotis ([email protected]) – Washington Lauren Lahey7, William Robinson7, Joshua Newsom5, Anne Stevens1,6 University School of Medicine, St Louis, Missouri, USA 1Department of Pediatrics, Division of Rheumatology, University of Pediatric Rheumatology 2016, 14(Suppl 1):P1 Washington, Seattle, WA, USA; 2Department of Oral Medicine, University of Washington, Seattle, WA, USA; 3Department of Rheumatology, Seattle Background Children's Hospital, Seattle, WA, USA; 4Department of Oral Health Evolving data link juvenile idiopathic arthritis (JIA) to environmental Sciences, University of Washington, Seattle, WA, USA; 5University of factors and gut microbes, which may trigger the innate immune sys- Washington, Seattle, WA, USA; 6Seattle Children's Research Institute, tem through bacterial lipopolysaccharides. We hypothesized that Seattle, WA, USA; 7Department of Medicine, Division of Immunology children with new onset JIA have increased intestinal bacterial trans- and Rheumatology, Stanford University, Stanford, CA, USA location and endotoxinemia. Correspondence: Sriharsha Grevich Methods ([email protected]) – Department of Pediatrics, 65 new onset, systemic treatment naive JIA patients (polyarticu- Division of Rheumatology, University of Washington, Seattle, WA, USA lar JIA, n = 21, oligoarticular JIA, n = 29 and spondylarthropathies, Pediatric Rheumatology 2016, 14(Suppl 1):P2 n = 15) and 14 healthy controls participated in the study. We determined the plasma immunoglobulin reactivity against Escher- Background ichia coli lipopolysaccharide (LPS). We measured the levels of Oral pathogens that cause periodontitis have been implicated as trig- lipopolysaccharide binding protein (LBP), and alpha-1-acid glyco- gers for rheumatoid arthritis (RA), with antibodies to bacterial citrulli- protein (A1AGP), which are acute phase proteins related to nated proteins (ACPA) suggested as a potential mechanism for the intestinal bacterial translocation, and C-reactive protein (CRP). transfer of oral inflammation to the joints. Although periodontitis is Assays were performed using commercial EIA kits (Hycult, R&D rare in children, gingivitis, present in 50 % of adolescents, is a systems) or laboratory-prepared LPS. chronic inflammatory precursor to periodontitis. Patients with juven- Results ile idiopathic arthritis (JIA) rarely produce ACPA, but patients with Children with polyarticular JIA have statistically significant in- polyarticular JIA who carry the ACPA, are considered to have more creased concentrations of circulating anti-LPS antibodies, LBP, aggressive arthritis, similar to adult RA patients. Because adult RA is CRP, and A1AGP compared to healthy controls (p < 0.05). The associated with gingival inflammation and periodontitis, we tested concentration of LBP, CRP and A1AGP in patients with polyarti- for an association between ACPA and dental clinical outcomes in JIA. cular JIA significantly differs from the oligoarticular JIA group Our study objectives were to test for increased frequency of gingi- (p < 0.05), but not spondylarthropathies. Spondylarthropathy vitis in children with JIA compared to controls, and to test for correla- patients have increased circulating anti-LPS antibodies com- tions between ACPA and dental clinical outcomes in JIA patients and pared to healthy controls (p < 0.05). There are no statistically dental controls. significant differences between oligoarticular JIA patients and Methods healthy controls. LBP and A1AGP levels correlate with CRP levels This was a cross-sectional study of 85 patients with JIA, 62 dental pa- (r=0.787andr=0.635respectively). tient controls and 11 healthy patient controls at the Seattle Children’s Conclusions Hospital (SCH) Rheumatology and Dental Clinics. Serum from an add- Children with polyarticular JIA and spondylarthropathies have evi- itional historic cohort of 30 healthy children was used to study ACPA. dence of increased exposure to gut bacteria, as reflected by anti- Rheumatologists and dentists completed the oral and joint exams LPS antibodies and LBP. The degree of exposure is proportional blinded to each other’s findings. ACPA were detected with a com- to the degree of systemic inflammation. These data imply that mercial CCP3 assay and also to 29 citrullinated full length proteins or the intestine maybe the source of stimulation for the immune peptides within these proteins using a custom Bio-Plex bead array. system in JIA. For each peptide, elevated levels were defined to be values larger © 2016 The Author(s). Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Pediatric Rheumatology 2016, Volume 14 Suppl 1 Page 2 of 16 than the maximum value observed for the healthy controls. Patients calcium binding proteins (13 %) and redox related proteins (10 %). were defined to have elevated ACPA if they had elevated levels for Furthermore, half of the identified target antigens represented mem- more than 4 of the proteins. The prevalence of elevated ACPA was brane proteins. Among the 738 candidate HAEC autoantigens were compared across groups using the chi-squared test. myosin light polypeptide 6 (MYL6) and myosin-9 (MYH9). IgG auto- Results antibodies to MYL6 were detected in 20 % of the patients with JDM Although JIA patients overall had better oral health than controls (n = 61) using ELISA assays. However, 50 % of the untreated JDM (lower indices for plaque, caries and gingivitis), they had signifi- patients with active disease (n = 10) had anti-MYL6 antibodies, in cantly more bleeding on probing of the gingiva, the most spe- contrast to 12 % (p < 0.05) of the patients with JIA (n = 17) and in cific sign of active inflammation (percentage of sites bleeding 16 % (p = 0.05) of control children (n = 25) tested on the same ELISA 17 % vs 8 %, p = 0.007). There was no correlation between JIA assays. IgG autoantibodies to MYH9 were detected in 31 % of the disease activity or immunosuppression with dental indices. ACPA active patients with JDM (n = 35), (50 % of the untreated JDM were detected in only three JIA patients by commercial CCP3 patients with active disease), in comparison to 27 % of the patients assay, but elevated levels were detected by the custom array in with JIA (n = 15) and 12 % (p < 0.05) of control children. 15/41 (37 %) of poly JIA, 14/36 (39 %) of oligo JIA, and 19/57 Conclusions (33 %) of dental controls. Antibodies to more than 4 citrullinated IgG antibodies to MYL6 and MYH9 were detected in the sera from peptides were most common in poly JIA 9/41 (22 %) compared patients with pediatric rheumatic diseases, respectively. These anti- with 1/36 (3 %) for oligo JIA, and 2/57 (4 %) for dental controls, bodies might be useful markers for pediatric rheumatic diseases. (p = 0.002 by chi-squared test). We found no associations be- Proteomic approaches are a powerful tool for identifying target anti- tween ACPA status and any dental index. gens for AECA. Conclusions Gingival inflammation was associated with JIA, suggesting a systemic P4 immune response could be triggered by oral bacteria involved in both oral and synovial inflammation. More sensitive and specific tests Transcriptional profiling reveals monocyte signature associated with JIA patient poor response to methotrexate for ACPA may lead to improved prognosis and understanding of the 1,2 2 1 1 triggers for arthritis in children. Halima Moncrieffe , Mark F. Bennett , Monica Tsoras , Lorie Luyrink , Huan Xu2, Sampath Prahalad3, Paula Morris4, Jason Dare4, Peter A. Nigrovic5, Margalit Rosenkranz6, Mara Becker7, Kathleen M. O’Neil8, P3 Thomas Griffin9, Daniel J. Lovell1, Alexei A. Grom1, Mario Medvedovic2, Novel autoantigens for endothelial cell antibodies in pediatric Susan D. Thompson1,2 rheumatic diseases identified
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