OBJECTIVE: To determine the association of polyunsaturated fatty acid (PUFA)-derived lipid mediators with progression from rheumatoid arthritis (RA)-related autoimmunity to inflammatory arthritis (IA). METHODS: We conducted a prospective cohort study using data from the Studies of the Etiology of Rheumatoid Arthritis (SERA). SERA enrolled first-degree relatives (FDRs) of individuals with RA (FDR cohort) and individuals who screened positive for RA-related autoantibodies at health fairs (screened cohort). We followed up 133 anti-cyclic citrullinated peptide 3.1 (anti-CCP3.1)-positive participants, 29 of whom developed IA. Lipid mediators selected a priori were quantified from stored plasma samples using liquid chromatography tandem mass spectrometry. We fit multivariable Cox proportional hazards models for each lipid mediator as a time-varying variable. For lipid mediators found to be significantly associated with IA, we then examined interleukin-1β (IL-1β), IL-6, IL-8, and tumor necrosis factor (TNF) as potential statistical mediators. RESULTS: For every 1 natural log pg/ml increase in the circulating plasma levels of proinflammatory 5-HETE, the risk of developing IA increased by 241% (hazard ratio 2.41 [95% confidence interval 1.43-4.07]) after adjusting for age at baseline, cohort (FDR or screened), and shared epitope status. The models examining 15-HETE and 17-HDHA had the same trend but did not reach significance. We did not find evidence that the association between 5-HETE and IA risk was influenced by the proinflammatory cytokines tested. CONCLUSION: In a prospective cohort of anti-CCP-positive individuals, higher levels of 5-HETE, an important precursor to proinflammatory leukotrienes, is associated with subsequent IA. Our findings highlight the potential significance of these PUFA metabolites in pre-RA populations.
OBJECTIVE: To determine the association of polyunsaturated fatty acid (PUFA)-derived lipid mediators with progression from rheumatoid arthritis (RA)-related autoimmunity to inflammatory arthritis (IA). METHODS: We conducted a prospective cohort study using data from the Studies of the Etiology of Rheumatoid Arthritis (SERA). SERA enrolled first-degree relatives (FDRs) of individuals with RA (FDR cohort) and individuals who screened positive for RA-related autoantibodies at health fairs (screened cohort). We followed up 133 anti-cyclic citrullinated peptide 3.1 (anti-CCP3.1)-positive participants, 29 of whom developed IA. Lipid mediators selected a priori were quantified from stored plasma samples using liquid chromatography tandem mass spectrometry. We fit multivariable Cox proportional hazards models for each lipid mediator as a time-varying variable. For lipid mediators found to be significantly associated with IA, we then examined interleukin-1β (IL-1β), IL-6, IL-8, and tumor necrosis factor (TNF) as potential statistical mediators. RESULTS: For every 1 natural log pg/ml increase in the circulating plasma levels of proinflammatory 5-HETE, the risk of developing IA increased by 241% (hazard ratio 2.41 [95% confidence interval 1.43-4.07]) after adjusting for age at baseline, cohort (FDR or screened), and shared epitope status. The models examining 15-HETE and 17-HDHA had the same trend but did not reach significance. We did not find evidence that the association between 5-HETE and IA risk was influenced by the proinflammatory cytokines tested. CONCLUSION: In a prospective cohort of anti-CCP-positive individuals, higher levels of 5-HETE, an important precursor to proinflammatory leukotrienes, is associated with subsequent IA. Our findings highlight the potential significance of these PUFA metabolites in pre-RA populations.
Authors: Kevin D Deane; Colin I O'Donnell; Wolfgang Hueber; Darcy S Majka; Ann A Lazar; Lezlie A Derber; William R Gilliland; Jess D Edison; Jill M Norris; William H Robinson; V Michael Holers Journal: Arthritis Rheum Date: 2010-11
Authors: Paola de Pablo; Dora Romaguera; Helena L Fisk; Philip C Calder; Anne-Marie Quirke; Alison J Cartwright; Salvatore Panico; Amalia Mattiello; Diana Gavrila; Carman Navarro; Carlotta Sacerdote; Paolo Vineis; Rosario Tumino; William E Ollier; Dominique S Michaud; Elio Riboli; Patrick J Venables; Benjamin A Fisher Journal: Ann Rheum Dis Date: 2018-02-07 Impact factor: 19.103
Authors: Wolfgang Hueber; Beren H Tomooka; Xiaoyan Zhao; Brian A Kidd; Jan W Drijfhout; James F Fries; Walther J van Venrooij; Allan L Metzger; Mark C Genovese; William H Robinson Journal: Ann Rheum Dis Date: 2006-08-10 Impact factor: 19.103
Authors: Jan M Hughes-Austin; Kevin D Deane; Lezlie A Derber; Jason R Kolfenbach; Gary O Zerbe; Jeremy Sokolove; Lauren J Lahey; Michael H Weisman; Jane H Buckner; Ted R Mikuls; James R O'Dell; Richard M Keating; Peter K Gregersen; William H Robinson; V Michael Holers; Jill M Norris Journal: Ann Rheum Dis Date: 2012-08-21 Impact factor: 19.103
Authors: K T Jørgensen; A Wiik; M Pedersen; C J Hedegaard; B F Vestergaard; R E Gislefoss; T K Kvien; J Wohlfahrt; K Bendtzen; M Frisch Journal: Ann Rheum Dis Date: 2007-07-20 Impact factor: 19.103
Authors: Patricia R Souza; Raquel M Marques; Esteban A Gomez; Romain A Colas; Roberta De Matteis; Anne Zak; Mital Patel; David J Collier; Jesmond Dalli Journal: Circ Res Date: 2019-12-12 Impact factor: 17.367
Authors: Lucy V Norling; Sarah E Headland; Jesmond Dalli; Hildur H Arnardottir; Oliver Haworth; Hefin R Jones; Daniel Irimia; Charles N Serhan; Mauro Perretti Journal: JCI Insight Date: 2016-04-21
Authors: Amir A Razmjou; Jennifer M Wang; Ani Shahbazian; Srinivasa Reddy; Christina Charles-Schoeman Journal: Clin Rheumatol Date: 2022-09-22 Impact factor: 3.650
Authors: Giulia Frazzei; Ronald F van Vollenhoven; Brigit A de Jong; Sarah E Siegelaar; Dirkjan van Schaardenburg Journal: Front Immunol Date: 2022-06-30 Impact factor: 8.786
Authors: Jung Hee Koh; Sang Jun Yoon; Mina Kim; Seonghun Cho; Johan Lim; Youngjae Park; Hyun-Sook Kim; Sung Won Kwon; Wan-Uk Kim Journal: Exp Mol Med Date: 2022-02-15 Impact factor: 12.153