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1. Smoking, Porphyromonas gingivalis and the immune response to citrullinated autoantigens before the clinical onset of rheumatoid arthritis in a Southern European nested case-control study.

Author

Fisher BA, Cartwright AJ, Quirke AM, de Pablo P, Romaguera D, Panico S, Mattiello A, Gavrila D, Navarro C, Sacerdote C, Vineis P, Tumino R, Lappin DF, Apatzidou D, Culshaw S, Potempa J, Michaud DS, Riboli E, and Venables PJ

Subjects
Adhesins, Bacterial immunology, Adult, Arthritis, Rheumatoid epidemiology, Arthritis, Rheumatoid microbiology, Autoantigens immunology, Case-Control Studies, Cysteine Endopeptidases immunology, Europe epidemiology, Female, Gingipain Cysteine Endopeptidases, Humans, Male, Middle Aged, Periodontitis complications, Periodontitis immunology, Prospective Studies, Protein-Arginine Deiminases, Smoking immunology, Arthritis, Rheumatoid immunology, Hydrolases immunology, Peptides, Cyclic immunology, Porphyromonas gingivalis enzymology, Smoking adverse effects
Abstract

Background: Antibodies to citrullinated proteins (ACPA) occur years before RA diagnosis. Porphyromonas gingivalis expresses its own peptidylarginine deiminase (PPAD), and is a proposed aetiological factor for the ACPA response. Smoking is a risk factor for both ACPA-positive RA and periodontitis. We aimed to study the relation of these factors to the risk of RA in a prospective cohort., Methods: We performed a nested case-control study by identifying pre-RA cases in four populations from the European Prospective Investigation into Cancer and nutrition, matched with three controls. Data on smoking and other covariates were obtained from baseline questionnaires. Antibodies to CCP2 and citrullinated peptides from α-enolase, fibrinogen, vimentin and PPAD were measured. Antibodies to arginine gingipain (RgpB) were used as a marker for P.gingivalis infection and validated in a separate cohort of healthy controls and subjects with periodontitis., Results: We studied 103 pre-RA cases. RA development was associated with several ACPA specificities, but not with antibodies to citrullinated PPAD peptides. Antibody levels to RgpB and PPAD peptides were higher in smokers but were not associated with risk of RA or with pre-RA autoimmunity. Former but not current smoking was associated with antibodies to α-enolase (OR 4.06; 95 % CI 1.02, 16.2 versus 0.54; 0.09-3.73) and fibrinogen peptides (OR 4.24; 95 % CI 1.2-14.96 versus 0.58; 0.13-2.70), and later development of RA (OR 2.48; 95 % CI 1.27-4.84 versus 1.57; 0.85-2.93), independent of smoking intensity., Conclusions: Smoking remains a risk factor for RA well before the clinical onset of disease. In this cohort, P.gingivalis is not associated with pre-RA autoimmunity or risk of RA in an early phase before disease-onset. Antibodies to PPAD peptides are not an early feature of ACPA ontogeny.

Published
2015
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2. Erratum to: Smoking, Porphyromonas gingivalis and the immune response to citrullinated autoantigens before the clinical onset of rheumatoid arthritis in a Southern European nested case-control study

Author

Benjamin A. Fisher, Alison J. Cartwright, Anne-Marie Quirke, Paola de Pablo, Dora Romaguera, Salvatore Panico, Amalia Mattiello, Diana Gavrila, Carmen Navarro, Carlotta Sacerdote, Paolo Vineis, Rosario Tumino, David F. Lappin, Danae Apatzidou, Shauna Culshaw, Jan Potempa, Dominique S. Michaud, Elio Riboli, Patrick J. Venables, Fisher, Benjamin A, Cartwright, Alison J, Quirke, Anne Marie, de Pablo, Paola, Romaguera, Dora, Panico, Salvatore, Mattiello, Amalia, Gavrila, Diana, Navarro, Carmen, Sacerdote, Carlotta, Vineis, Paolo, Tumino, Rosario, Lappin, David F, Apatzidou, Danae, Culshaw, Shauna, Potempa, Jan, Michaud, Dominique S, Riboli, Elio, and Venables, Patrick J.

Subjects
Adult, Male, Hydrolases, Autoantigens, Peptides, Cyclic, Arthritis, Rheumatoid, Rheumatology, Humans, Orthopedics and Sports Medicine, Prospective Studies, Adhesins, Bacterial, Periodontitis, Science & Technology, Smoking, 1103 Clinical Sciences, Middle Aged, Europe, Cysteine Endopeptidases, Orthopedics, Case-Control Studies, Gingipain Cysteine Endopeptidases, Protein-Arginine Deiminases, Female, Erratum, Porphyromonas gingivalis, Life Sciences & Biomedicine
Abstract

Antibodies to citrullinated proteins (ACPA) occur years before RA diagnosis. Porphyromonas gingivalis expresses its own peptidylarginine deiminase (PPAD), and is a proposed aetiological factor for the ACPA response. Smoking is a risk factor for both ACPA-positive RA and periodontitis. We aimed to study the relation of these factors to the risk of RA in a prospective cohort.We performed a nested case-control study by identifying pre-RA cases in four populations from the European Prospective Investigation into Cancer and nutrition, matched with three controls. Data on smoking and other covariates were obtained from baseline questionnaires. Antibodies to CCP2 and citrullinated peptides from α-enolase, fibrinogen, vimentin and PPAD were measured. Antibodies to arginine gingipain (RgpB) were used as a marker for P.gingivalis infection and validated in a separate cohort of healthy controls and subjects with periodontitis.We studied 103 pre-RA cases. RA development was associated with several ACPA specificities, but not with antibodies to citrullinated PPAD peptides. Antibody levels to RgpB and PPAD peptides were higher in smokers but were not associated with risk of RA or with pre-RA autoimmunity. Former but not current smoking was associated with antibodies to α-enolase (OR 4.06; 95 % CI 1.02, 16.2 versus 0.54; 0.09-3.73) and fibrinogen peptides (OR 4.24; 95 % CI 1.2-14.96 versus 0.58; 0.13-2.70), and later development of RA (OR 2.48; 95 % CI 1.27-4.84 versus 1.57; 0.85-2.93), independent of smoking intensity.Smoking remains a risk factor for RA well before the clinical onset of disease. In this cohort, P.gingivalis is not associated with pre-RA autoimmunity or risk of RA in an early phase before disease-onset. Antibodies to PPAD peptides are not an early feature of ACPA ontogeny.

Published
2016

3. Smoking, Porphyromonas gingivalis and the immune response to citrullinated autoantigens before the clinical onset of rheumatoid arthritis in a Southern European nested case-control study

Author

Danae Apazidou, Salvatore Panico, Jan Potempa, Amalia Mattiello, Elio Riboli, Paolo Vineis, Anne-Marie Quirke, Paola de Pablo, Shauna Culshaw, Patrick J Venables, Benjamin A Fisher, Carmen Navarro, Dora Romaguera, Rosario Tumino, David F. Lappin, Carlotta Sacerdote, Dominique S. Michaud, Alison J Cartwright, Diana Gavrila, Fisher, Benjamin A, Cartwright, Alison J, Quirke, Anne Marie, de Pablo, Paola, Romaguera, Dora, Panico, Salvatore, Mattiello, Amalia, Gavrila, Diana, Navarro, Carmen, Sacerdote, Carlotta, Vineis, Paolo, Tumino, Rosario, Lappin, David F, Apatzidou, Danae, Apazidou, Danae, Culshaw, Shauna, Potempa, Jan, Michaud, Dominique S, Riboli, Elio, and Venables, Patrick J.

Subjects
Male, autoantígenos, Hydrolases, humanos, Porphyromonas gingivali, Autoantigens, UNAFFECTED 1ST-DEGREE RELATIVES, Arthritis, Rheumatoid, HLA-DRB1 SHARED EPITOPE, estudios prospectivos, Orthopedics and Sports Medicine, Prospective Studies, rheumatoid arthritis (RA), Prospective cohort study, mediana edad, cisteína endopeptidasas, Periodontiti, Smoking, Citrullination, adulto, Middle Aged, anti-citrullinated proteinantibodies (ACPA), 3. Good health, European Prospective Investigation into Cancer and Nutrition, Europe, Cysteine Endopeptidases, Rheumatoid arthritis, Female, Case-Control Studie, Life Sciences & Biomedicine, Porphyromonas gingivalis, Research Article, Human, Adult, citrullination, estudios de casos y controles, Hydrolase, Peptides, Cyclic, smoking, Rheumatology, Autoantigen, medicine, Humans, ARGININE DEIMINASE TYPE-4, Risk factor, Periodontitis, Adhesins, Bacterial, PEPTIDYLARGININE DEIMINASE, Science & Technology, business.industry, Arthritis, COLLAGEN-INDUCED ARTHRITIS, Case-control study, PERIODONTAL-DISEASE, hábito de fumar, medicine.disease, ALPHA-ENOLASE, ANTICITRULLINATED PROTEIN ANTIBODIES, hidrolasas, Prospective Studie, Orthopedics, FINE-SPECIFICITY, Case-Control Studies, Rheumatoid arthritis (RA), Anti-citrullinated protein antibodies (ACPA), péptidos, Nested case-control study, Immunology, CIGARETTE-SMOKING, Peptides, business, artritis, Cysteine Endopeptidase
Abstract

Background: Antibodies to citrullinated proteins (ACPA) occur years before RA diagnosis. Porphyromonas gingivalis expresses its own peptidylarginine deiminase (PPAD), and is a proposed aetiological factor for the ACPA response. Smoking is a risk factor for both ACPA-positive RA and periodontitis. We aimed to study the relation of these factors to the risk of RA in a prospective cohort. Methods: We performed a nested case-control study by identifying pre-RA cases in four populations from the European Prospective Investigation into Cancer and nutrition, matched with three controls. Data on smoking and other covariates were obtained from baseline questionnaires. Antibodies to CCP2 and citrullinated peptides from a-enolase, fibrinogen, vimentin and PPAD were measured. Antibodies to arginine gingipain (RgpB) were used as a marker for P. gingivalis infection and validated in a separate cohort of healthy controls and subjects with periodontitis. Results: We studied 103 pre-RA cases. RA development was associated with several ACPA specificities, but not with antibodies to citrullinated PPAD peptides. Antibody levels to RgpB and PPAD peptides were higher in smokers but were not associated with risk of RA or with pre-RA autoimmunity. Former but not current smoking was associated with antibodies to a-enolase (OR 4.06; 95 % CI 1.02, 16.2 versus 0.54; 0.09-3.73) and fibrinogen peptides (OR 4.24; 95 % CI 1.2-14.96 versus 0.58; 0.13-2.70), and later development of RA (OR 2.48; 95 % CI 1.27-4.84 versus 1.57; 0.85-2.93), independent of smoking intensity. Conclusions: Smoking remains a risk factor for RA well before the clinical onset of disease. In this cohort, P. gingivalis is not associated with pre-RA autoimmunity or risk of RA in an early phase before disease-onset. Antibodies to PPAD peptides are not an early feature of ACPA ontogeny., Funding was received from the Imperial College London National Institute of Health Research (NIHR) Biomedical Research Centre, and from the European Union funded IMI project 'BeTheCure' (contract number 115142-2) and FP7 grant 'Gums & Joints' (HEALTH-F2-2010-261460). JP acknowledges support by grant DE 022597 from NIH/NIDCR.

Published
2015

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