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Johansson, Linda
Publikationer (10 of 22) Visa alla publikationer
Michailidou, D., Johansson, L., Kuley, R., Wang, T., Hermanson, P., Rantapää-Dahlqvist, S. & Lood, C. (2023). Immune complex-mediated neutrophil activation in patients with polymyalgia rheumatica. Rheumatology, 62(8), 2880-2886
Öppna denna publikation i ny flik eller fönster >>Immune complex-mediated neutrophil activation in patients with polymyalgia rheumatica
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2023 (Engelska)Ingår i: Rheumatology, ISSN 1462-0324, E-ISSN 1462-0332, Vol. 62, nr 8, s. 2880-2886Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

OBJECTIVE: Neutrophils are important in host defence. However, neutrophils are also linked to inflammation and organ damage. The purpose of this study was to assess whether markers of neutrophil activation are increased in PMR.

METHODS: Levels of immune complexes (IC), calprotectin and neutrophil extracellular traps (NETs) were measured in plasma of healthy individuals (n = 30) and patients with PMR (n = 60), at flare and upon treatment with glucocorticoids using ELISA. Plasma-mediated neutrophil activation was assessed in presence of an FcγRIIA inhibitory antibody (IV.3).

RESULTS: Plasma levels of calprotectin and NETs were elevated in PMR (P < 0.001). Mechanistically, neutrophil activation was driven by ICs, present in plasma, able to up-regulate neutrophil activation markers CD66b and CD11b (P < 0.0001) in an FcγRIIA-dependent manner (P < 0.01). Of note, circulating levels of IC correlated with plasma induced CD66b and CD11b (r = 0.51, P = 0.004, and r = 0.46, P = 0.01, respectively) and decreased after glucocorticoid therapy. In contrast to NETs, calprotectin significantly decreased after glucocorticoid therapy (P < 0.001) and was higher in PMR without overlapping GCA compared with patients with overlapping disease (P = 0.014). Interestingly, musculoskeletal involvement was associated with elevated levels of calprotectin before initiation of glucocorticoid therapy (P = 0.036).

CONCLUSIONS: Neutrophil activation, including NET formation, is increased in PMR, through IC-mediated engagement of FcγRIIA. Clinically, neutrophil activation is associated with musculoskeletal involvement, with calprotectin, but not NETs, being a biomarker of treatment response in PMR patients. In all, IC-mediated neutrophil activation is a central process in PMR pathogenesis identifying potential novel therapeutic targets (FcγRIIA), as well as soluble markers for disease monitoring (calprotectin).

Ort, förlag, år, upplaga, sidor
Oxford University Press, 2023
Nyckelord
calprotectin, immune complexes, neutrophil extracellular traps, neutrophils, PMR
Nationell ämneskategori
Reumatologi och inflammation
Identifikatorer
urn:nbn:se:umu:diva-212736 (URN)10.1093/rheumatology/keac722 (DOI)000908331800001 ()36562570 (PubMedID)2-s2.0-85162077877 (Scopus ID)
Tillgänglig från: 2023-08-14 Skapad: 2023-08-14 Senast uppdaterad: 2023-08-14Bibliografiskt granskad
Li, T., Ge, C., Krämer, A., Sareila, O., Leu Agelii, M., Johansson, L., . . . Holmdahl, R. (2023). Pathogenic antibody response to glucose-6-phosphate isomerase targets a modified epitope uniquely exposed on joint cartilage. Annals of the Rheumatic Diseases, 82(6), 799-808
Öppna denna publikation i ny flik eller fönster >>Pathogenic antibody response to glucose-6-phosphate isomerase targets a modified epitope uniquely exposed on joint cartilage
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2023 (Engelska)Ingår i: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 82, nr 6, s. 799-808Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Objectives: To identify the arthritogenic B cell epitopes of glucose-6-phosphate isomerase (GPI) and their association with rheumatoid arthritis (RA).

Methods: IgG response towards a library of GPI peptides in patients with early RA, pre-symptomatic individuals and population controls, as well as in mice, were tested by bead-based multiplex immunoassays and ELISA. Monoclonal IgG were generated, and the binding specificity and affinity were determined by ELISA, gel size exclusion chromatography, surface plasma resonance and X-ray crystallography. Arthritogenicity was investigated by passive transfer experiments. Antigen-specific B cells were identified by peptide tetramer staining.

Results: Peptide GPI293-307 was the dominant B cell epitope in K/BxN and GPI-immunised mice. We could detect B cells and low levels of IgM antibodies binding the GPI293-307 epitopes, and high affinity anti-GPI293-307 IgG antibodies already 7 days after GPI immunisation, immediately before arthritis onset. Transfer of anti-GPI293-307 IgG antibodies induced arthritis in mice. Moreover, anti-GPI293-307 IgG antibodies were more frequent in individuals prior to RA onset (19%) than in controls (7.5%). GPI293-307-specific antibodies were associated with radiographic joint damage. Crystal structures of the Fab-peptide complex revealed that this epitope is not exposed in native GPI but requires conformational change of the protein in inflamed joint for effective recognition by anti-GPI293-307 antibodies.

Conclusions: We have identified the major pathogenic B cell epitope of the RA-associated autoantigen GPI, at position 293-307, exposed only on structurally modified GPI on the cartilage surface. B cells to this neo-epitope escape tolerance and could potentially play a role in the pathogenesis of RA.

Ort, förlag, år, upplaga, sidor
BMJ Publishing Group Ltd, 2023
Nyckelord
arthritis, experimental, arthritis, rheumatoid, autoantibodies, autoimmunity, inflammation
Nationell ämneskategori
Immunologi inom det medicinska området Reumatologi och inflammation
Identifikatorer
urn:nbn:se:umu:diva-206885 (URN)10.1136/ard-2022-223633 (DOI)000951597300001 ()36858822 (PubMedID)2-s2.0-85152199960 (Scopus ID)
Forskningsfinansiär
Knut och Alice Wallenbergs Stiftelse, 2019.0059Vetenskapsrådet, 2019-01209Vetenskapsrådet, 2019- 01140Reumatikerförbundet, 931878Reumatikerförbundet, 757331
Tillgänglig från: 2023-04-20 Skapad: 2023-04-20 Senast uppdaterad: 2023-07-13Bibliografiskt granskad
Kokkonen, H., Johansson, L., Stenlund, H. & Rantapää-Dahlqvist, S. (2022). Cardiovascular risk factors before onset of rheumatoid arthritis are associated with cardiovascular events after disease onset: a case–control study. Journal of Clinical Medicine, 11(21), Article ID 6535.
Öppna denna publikation i ny flik eller fönster >>Cardiovascular risk factors before onset of rheumatoid arthritis are associated with cardiovascular events after disease onset: a case–control study
2022 (Engelska)Ingår i: Journal of Clinical Medicine, E-ISSN 2077-0383, Vol. 11, nr 21, artikel-id 6535Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Background: The increased comorbidity and mortality in rheumatoid arthritis (RA) patients are largely due to cardiovascular disease (CVD). Previously, we demonstrated increased frequencies of risk factors for CVD (elevated body mass index (BMI), elevated apoliprotein (Apo) B:ApoA1 ratio, and smoking) in pre-RA individuals compared with matched controls. Objectives: Assess the impact of traditional CV risk factors present before the onset of RA on the risk of CV events (CVE) after diagnosis in comparison with matched controls. Methods: A case–control study including 521 pre-symptomatic individuals and 1566 controls identified within the Health Surveys of the Medical Biobank was performed. CVD risk factors were hypertension, elevated ApoB:A1 ratio, BMI, diabetes, and smoking. Information on comorbidities was requested from the Swedish National Patient Register and Cause of Death Register. Results: Pre-RA individuals had a higher risk of future CVE compared with matched controls (HR [95% CI] 1.70 [1.31–2.21]), which remained after adjustments for risk factors for CVD (HR [95% CI] 1.73 [1.27–2.35]). Most risk factors were associated with CVE after diagnosis, and a combination resulted in a higher risk in RA compared with controls; two risk factors, HR [95% CI] 2.70 [1.19–6.13] vs. 1.26 [0.75–2.13]; and three to four risk factors, HR [95% CI] 6.32 [2.92–13.68] vs. 3.77 [2.34–6.00]. Conclusions: Risk factors for CVD present in pre-RA individuals were associated with future CVE, and even after adjustments for these risk factors and treatments after RA onset, pre-RA individuals had a higher risk of CVE compared with controls. These findings further highlight the importance of the early assessment of risk for CVD.

Ort, förlag, år, upplaga, sidor
MDPI, 2022
Nyckelord
cardiovascular disease, rheumatoid arthritis, risk factors
Nationell ämneskategori
Kardiologi Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi
Identifikatorer
urn:nbn:se:umu:diva-201228 (URN)10.3390/jcm11216535 (DOI)000883465600001 ()36362763 (PubMedID)2-s2.0-85141656161 (Scopus ID)
Forskningsfinansiär
Vetenskapsrådet, 2018-02551Stiftelsen Konung Gustaf V:s 80-årsfondReumatikerförbundetUmeå universitetRegion Västerbotten
Tillgänglig från: 2022-12-01 Skapad: 2022-12-01 Senast uppdaterad: 2022-12-01Bibliografiskt granskad
Johansson, L., Berglin, E., Eriksson, O., Mohammad, A., Dahlqvist, J. & Rantapää-Dahlqvist, S. (2022). Complement activation prior to symptom onset in myeloperoxidase ANCA-associated vasculitis but not proteinase 3 ANCA associated vasculitis: a Swedish biobank study. Scandinavian Journal of Rheumatology, 51(3), 214-219
Öppna denna publikation i ny flik eller fönster >>Complement activation prior to symptom onset in myeloperoxidase ANCA-associated vasculitis but not proteinase 3 ANCA associated vasculitis: a Swedish biobank study
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2022 (Engelska)Ingår i: Scandinavian Journal of Rheumatology, ISSN 0300-9742, E-ISSN 1502-7732, Vol. 51, nr 3, s. 214-219Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Objective: Increased soluble levels of complement effectors have been demonstrated in active anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), but the timing of complement activation in the autoimmune inflammation remains elusive. This study investigated whether the complement system is activated before onset of symptoms in AAV.

Method: The Swedish National Patient Register and Cause of Death register were linked to registers of five biobanks to identify individuals sampled before AAV symptom onset. Diagnosis of AAV and time-point for symptom onset were confirmed by reviewing medical records. We identified 64 presymptomatic individuals with serum samples > 1 month < 10 years from AAV symptom onset and 122 matched controls. Complement factors (C2, C5) and activation markers (C5a, C4b) were measured using Luminex technology.

Results: Presymptomatic individuals had higher levels of C5 up to 6.5 years before symptom onset, compared with controls [median (IQR) 80.7 (131.9) vs 46.6 (63.4) µg/mL, p = 0.05]. Levels of C5a increased significantly during the pre-dating time (p = 0.033) until symptom onset. The complement levels were significantly higher in presymptomatic myeloperoxidase (MPO)-ANCA+ individuals versus MPO-ANCAand proteinase-3-ANCA+ individuals. C5 was significantly increased in cases with renal involvement at diagnosis versus controls (p = 0.022), whereas levels of both C5 and C5a were significantly increased in presymptomatic individuals diagnosed with microscopic polyangiitis after onset compared with controls (C5: p = 0.027; C5a: p = 0.027).

Conclusion: Activation of the complement system is an early event in the pathogenesis of AAV and is mainly associated with MPO-ANCA+ AAV and with microscopic polyangiitis.

Ort, förlag, år, upplaga, sidor
Taylor & Francis Group, 2022
Nationell ämneskategori
Reumatologi och inflammation
Forskningsämne
reumatologi
Identifikatorer
urn:nbn:se:umu:diva-192169 (URN)10.1080/03009742.2021.1989814 (DOI)000744923100001 ()35048784 (PubMedID)2-s2.0-85123416847 (Scopus ID)
Tillgänglig från: 2022-02-03 Skapad: 2022-02-03 Senast uppdaterad: 2022-07-08Bibliografiskt granskad
Esberg, A., Johansson, L., Berglin, E., Mohammad, A. J., Jonsson, A. P., Dahlqvist, J., . . . Rantapää-Dahlqvist, S. (2022). Oral Microbiota Profile in Patients with Anti-Neutrophil Cytoplasmic Antibody–Associated Vasculitis. Microorganisms, 10(8), Article ID 1572.
Öppna denna publikation i ny flik eller fönster >>Oral Microbiota Profile in Patients with Anti-Neutrophil Cytoplasmic Antibody–Associated Vasculitis
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2022 (Engelska)Ingår i: Microorganisms, E-ISSN 2076-2607, Vol. 10, nr 8, artikel-id 1572Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Microbiota has been associated with autoimmune diseases, with nasal Staphylococcus aureus being implicated in the pathogenesis of anti-neutrophil cytoplasmic antibody–associated vasculitis (AAV). Little is known about the role of oral microbiota in AAV. In this study, levels of IgG antibodies to 53 oral bacterial species/subspecies were screened using immunoblotting in plasma/serum in pre-symptomatic AAV-individuals (n = 85), matched controls, and established AAV-patients (n = 78). Saliva microbiota from acute-AAV and controls was sequenced from 16s rDNA amplicons. Information on dental status was extracted from a national register. IgG levels against oral bacteria were lower in established AAV versus pre-AAV and controls. Specifically, pre-AAV samples had, compared to controls, a higher abundance of periodontitis-associated species paralleling more signs of periodontitis in established AAV-patients than controls. Saliva microbiota in acute-AAV showed higher within-sample diversity but fewer detectable amplicon-sequence variants and taxa in their core microbiota than controls. Acute-AAV was not associated with increased abundance of periodontal bacteria but species in, e.g., Arthrospira, Staphylococcus, Lactobacillus, and Scardovia. In conclusion, the IgG profiles against oral bacteria differed between pre-AAV, established AAV, and controls, and microbiota profiles between acute AAV and controls. The IgG shift from a pre-symptomatic stage to established disease cooccurred with treatment of immunosuppression and/or antibiotics.

Ort, förlag, år, upplaga, sidor
MDPI, 2022
Nyckelord
anti-neutrophil cytoplasmatic antibody–associated vasculitis, caries, granulomatosis with polyangiitis (GPA), IgG, microscopic polyangiitis (MPA), myeloperoxidase (MPO)-ANCA, oral microbiota, periodontal disease, proteinase 3 (PR3)-ANCA, vasculitis
Nationell ämneskategori
Medicinsk bioteknologi (med inriktning mot cellbiologi (inklusive stamcellsbiologi), molekylärbiologi, mikrobiologi, biokemi eller biofarmaci)
Identifikatorer
urn:nbn:se:umu:diva-199365 (URN)10.3390/microorganisms10081572 (DOI)000845508000001 ()36013990 (PubMedID)2-s2.0-85137345895 (Scopus ID)
Forskningsfinansiär
Vetenskapsrådet, 2018-02551
Tillgänglig från: 2022-11-03 Skapad: 2022-11-03 Senast uppdaterad: 2023-05-24Bibliografiskt granskad
Zhang, Y., Johansson, L., Andersson-Assarsson, J., Taube, M., Peltonen, M., Svensson, P.-A., . . . Maglio, C. (2021). Adiponectin Associates with Rheumatoid Arthritis Risk in Overweight and Obesity Independently of Other Adipokines. Journal of Clinical Medicine, 10(13), Article ID 2791.
Öppna denna publikation i ny flik eller fönster >>Adiponectin Associates with Rheumatoid Arthritis Risk in Overweight and Obesity Independently of Other Adipokines
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2021 (Engelska)Ingår i: Journal of Clinical Medicine, E-ISSN 2077-0383, Vol. 10, nr 13, artikel-id 2791Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

We recently reported that increased serum adiponectin was associated with rheumatoid arthritis (RA) risk in subjects with obesity. We hereby aim to determine if other adipokines associate with RA risk and if the association between adiponectin and RA is independent of other adipokines. Two nested-case control studies were performed in two different cohorts: 82 participants of the Swedish Obese Subjects (SOS) study who developed RA during follow-up matched with 410 controls, and 88 matched pairs from the Medical Biobank of Northern Sweden. Baseline levels of circulating adipokines were measured using ELISA. In a multivariable analysis in the SOS cohort, higher adiponectin was associated with an increased risk of RA independently of other adipokines (OR for RA risk: 1.06, 95% CI: 1.01-1.12, p = 0.02). No association between leptin, resistin, and visfatin levels and the risk of RA was detected. In the cohort from the Medical Biobank of Northern Sweden, higher adiponectin was associated with an increased risk of RA only in participants with overweight/obesity (OR: 1.17, 95% CI: 1.01-1.36, p = 0.03), independently of other adipokines. Our results show that in individuals with overweight/obesity, higher circulating levels of adiponectin, but not leptin, resistin, or visfatin, were associated with an increased RA risk.

Ort, förlag, år, upplaga, sidor
MDPI, 2021
Nyckelord
adiponectin, adipokines, rheumatology, obesity, overweight, case control study
Nationell ämneskategori
Reumatologi och inflammation
Identifikatorer
urn:nbn:se:umu:diva-187300 (URN)10.3390/jcm10132791 (DOI)000671146300001 ()34201946 (PubMedID)2-s2.0-85114071015 (Scopus ID)
Forskningsfinansiär
Knut och Alice Wallenbergs StiftelseVetenskapsrådet, 2018-02551Stiftelsen Konung Gustaf V:s 80-årsfondKonung Gustaf V:s och Drottning Victorias FrimurarestiftelseReumatikerförbundet
Tillgänglig från: 2021-09-08 Skapad: 2021-09-08 Senast uppdaterad: 2023-03-24Bibliografiskt granskad
Berglin, E., Mohammad, A. J., Dahlqvist, J., Johansson, L., Eriksson, C., Sjöwall, J. & Rantapää-Dahlqvist, S. (2021). Anti-neutrophil cytoplasmic antibodies predate symptom onset of ANCA-associated vasculitis: a case-control study. Journal of Autoimmunity, 117, Article ID 102579.
Öppna denna publikation i ny flik eller fönster >>Anti-neutrophil cytoplasmic antibodies predate symptom onset of ANCA-associated vasculitis: a case-control study
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2021 (Engelska)Ingår i: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 117, artikel-id 102579Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Objectives: Anti-neutrophil cytoplasmic autoantibodies [ANCA) are important for diagnosis of ANCA-associated vasculitides (AAV). The timing of antibody development is not well established. To investigate the development of proteinase 3 (PR3)- and myeloperoxidase (MPO)-ANCA, blood samples collected before onset of symptoms of AAV were analysed.

Methods: To identify AAV patients with blood samples predating symptoms, the National Patient Register and Cause of Death register were scrutinized for ICD codes for AAV and linked to the registers of five biobanks. Diagnoses of AAV and time point for symptom onset were confirmed by reviewing 504 case-record. Eighty-five AAV cases (34 males, 51 females) with samples >1 month < 10 years from AAV symptom onset and two controls matched for sex, age, and sampling time for each case were included. Samples were screened using ELISAs for ANCA and further analysed for PR3-or MPO- specificities.

Results: In ANCA-screen 35.7% of the pre-symptomatic cases and 3.5% of controls tested positive (p < 0.01). 26.2% of the cases were PR3-ANCA+ and 10.7% MPO-ANCA+. Median (Q1-Q3) predating time for PR3-ANCA+ was 2.7 (0.3–7.7) years and MPO-ANCA+ 2.0 (0.9–3.5) years. PR3-ANCA was demonstrated in samples up to nine years before symptom onset. At symptom onset predating PR3-ANCA+ cases were younger than PR3-ANCA- (P < 0.01), and MPO-ANCA+ were older than MPO-ANCA- (p < 0.05). Predating MPO-ANCA+ cases vs. MPO-ANCA- and vs. PR3-ANCA+ cases had more often at symptoms onset manifestations from lungs, kidneys or peripheral nervous system (p < 0.01 and p < 0.05, respectively).

Conclusion: The PR3-and MPO-ANCAs are present years before AAV symptom onset and represent distinct diseases.

Ort, förlag, år, upplaga, sidor
Elsevier, 2021
Nyckelord
AAV, GPA, MPA, MPO-ANCA, PR3-ANCA, Predate symptom onset
Nationell ämneskategori
Reumatologi och inflammation Urologi och njurmedicin
Identifikatorer
urn:nbn:se:umu:diva-212005 (URN)10.1016/j.jaut.2020.102579 (DOI)000614250900003 ()33340843 (PubMedID)2-s2.0-85097887786 (Scopus ID)
Forskningsfinansiär
Vetenskapsrådet, 2018-02551Stiftelsen Konung Gustaf V:s 80-årsfondReumatikerförbundetUmeå universitet
Tillgänglig från: 2023-07-12 Skapad: 2023-07-12 Senast uppdaterad: 2023-07-12Bibliografiskt granskad
Juneblad, K., Kastbom, A., Johansson, L., Rantapää-Dahlqvist, S., Söderkvist, P. & Alenius, G.-M. (2021). Association between inflammasome-related polymorphisms and psoriatic arthritis. Scandinavian Journal of Rheumatology, 50(3), 206-212
Öppna denna publikation i ny flik eller fönster >>Association between inflammasome-related polymorphisms and psoriatic arthritis
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2021 (Engelska)Ingår i: Scandinavian Journal of Rheumatology, ISSN 0300-9742, E-ISSN 1502-7732, Vol. 50, nr 3, s. 206-212Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Objective: Psoriatic arthritis (PsA) is a heterogeneous inflammatory disease associated with psoriasis. Underlying genetic factors are considered important for disease expression and prognosis of PsA. Interleukin-1 beta-regulating protein complexes called inflammasomes are associated with several inflammatory diseases, e.g. rheumatoid arthritis and psoriasis. The aim was to determine whether inflammasome-related genetic variation is associated with PsA susceptibility or different disease phenotypes.

Method: DNA from 724 patients with PsA and 587 population-based controls from northern Sweden was analysed for single-nucleotide polymorphisms in NLRP3-Q750K (rs35829419), NLRP3 (rs10733113), CARD8-C10X (rs2043211), NLRP1 (rs8079034), and NLRP1 (rs878329).

Results: Significant associations were found with the genotype AA (vs AT+TT) of rs2043211 for PsA patients compared with controls [odds ratio (OR), 95% confidence interval (CI) 1.32 (1.05-1.65), p = 0.016]; and between the C-allele of rs878329 and axial involvement of PsA [OR (95% CI) 1.37 (1.02-1.84), p = 0.035], the T-allele of rs8079034 with prescription of conventional synthetic disease-modifying anti-rheumatic drugs [OR (95% CI) 1.76 (1.23-2.53), p = 0.0020], the G-allele of rs10733113 and patients with a skin disease with early onset [OR (95% CI) 1.58 (1.13-2.21), p = 0.007], and the C-allele of rs35829419 and a destructive/deforming disease [OR (95% CI) 1.63 (1.04-2.55), p = 0.030].

Conclusions: This study is the first to show an association with a genetic polymorphism in an inflammasome-related gene, CARD8-C10X (rs2043211), in patients with PsA. Associations between different phenotypes of PsA and different polymorphisms of the inflammasome genes were also found. Our results indicate the involvement of inflammasome genes in the pathogenesis and disease expression of PsA.

Ort, förlag, år, upplaga, sidor
Taylor & Francis, 2021
Nationell ämneskategori
Reumatologi och inflammation
Identifikatorer
urn:nbn:se:umu:diva-178339 (URN)10.1080/03009742.2020.1834611 (DOI)000597863100001 ()33300400 (PubMedID)2-s2.0-85105904969 (Scopus ID)
Forskningsfinansiär
Västerbottens läns landsting
Tillgänglig från: 2021-01-11 Skapad: 2021-01-11 Senast uppdaterad: 2023-03-23Bibliografiskt granskad
Esberg, A., Johansson, L., Johansson, I. & Rantapää-Dahlqvist, S. (2021). Oral microbiota identifies patients in early onset rheumatoid arthritis. Microorganisms, 9(8), Article ID 1657.
Öppna denna publikation i ny flik eller fönster >>Oral microbiota identifies patients in early onset rheumatoid arthritis
2021 (Engelska)Ingår i: Microorganisms, E-ISSN 2076-2607, Vol. 9, nr 8, artikel-id 1657Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Rheumatoid arthritis (RA) is the most common autoimmune inflammatory disease, and single periodontitis-associated bacteria have been suggested in disease manifestation. Here, the oral microbiota was characterized in relation to the early onset of RA (eRA) taking periodontal status into consideration. 16S rRNA gene amplicon sequencing of saliva bacterial DNA from 61 eRA patients without disease-modifying anti-rheumatic drugs and 59 matched controls was performed. Taxonomic classification at 98.5% was conducted against the Human Oral Microbiome Database, microbiota functions were predicted using PICRUSt, and periodontal status linked from the Swedish quality register for clinically assessed caries and periodontitis. The participants were classified into three distinct microbiota-based cluster groups with cluster allocation differences by eRA status. Independently of periodontal status, eRA patients had enriched levels of Prevotella pleuritidis, Treponema denticola, Porphyromonas endodontalis and Filifactor alocis species and in the Porphyromonas and Fusobacterium genera and functions linked to ornithine metabolism, glucosylceramidase, beta-lactamase resistance, biphenyl degradation, fatty acid metabolism and 17-beta-estradiol-17-dehydrogenase metabolism. The results support a deviating oral microbiota composition already in eRA patients compared with healthy controls and highlight a panel of oral bacteria that may be useful in eRA risk assessment in both periodontally healthy and diseased persons.

Ort, förlag, år, upplaga, sidor
MDPI, 2021
Nyckelord
16S rDNA sequencing, Oral microbiota, Periodontitis, Rheumatoid arthritis
Nationell ämneskategori
Odontologi
Identifikatorer
urn:nbn:se:umu:diva-186552 (URN)10.3390/microorganisms9081657 (DOI)000689454000001 ()2-s2.0-85111635486 (Scopus ID)
Tillgänglig från: 2021-08-16 Skapad: 2021-08-16 Senast uppdaterad: 2023-09-05Bibliografiskt granskad
Gomez-Bañuelos, E., Johansson, L., Konig, M. F., Lundquist, A., Paz, M., Buhlin, K., . . . Andrade, F. (2020). Exposure to Aggregatibacter Actinomycetemcomitans before Symptom Onset and the Risk of Evolving to Rheumatoid Arthritis. Journal of Clinical Medicine, 9(6), Article ID 1906.
Öppna denna publikation i ny flik eller fönster >>Exposure to Aggregatibacter Actinomycetemcomitans before Symptom Onset and the Risk of Evolving to Rheumatoid Arthritis
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2020 (Engelska)Ingår i: Journal of Clinical Medicine, E-ISSN 2077-0383, Vol. 9, nr 6, artikel-id 1906Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Periodontal disease has been implicated in the pathogenesis of rheumatoid arthritis (RA), an autoimmune disease characterized by immune-mediated synovial damage, and antibodies to citrullinated antigens. Here, we investigate the association between exposure to the periodontal pathogen Aggregatibacter actinomycetemcomitans (Aa) and the development of RA. IgM, IgG and IgA antibodies to Aa leukotoxin A (LtxA) were detected by ELISA in plasma from a cohort of Swedish adults at different stages of RA development, from before onset of symptoms to established disease. Patients with early and established RA had increased levels of anti-LtxA IgM compared with matched non-RA controls and periodontally healthy individuals. Logistic regression revealed that anti-LtxA IgM levels were associated with RA during early disease (OR 1.012, 95%CI 1.007, 1.017), which was maintained after adjustment for smoking, anti-CCP antibodies, rheumatoid factor, HLA-DRB1 shared epitope alleles and sex. We found no association between anti-LtxA IgG/IgA antibodies and RA at any stage of disease development. The data support a temporal association between anti-LtxA IgM antibodies and the development of RA, suggesting that a subset of RA patients may have been exposed to Aa around the time of transition from being asymptomatic to become a patient with RA.

Ort, förlag, år, upplaga, sidor
Basel: MDPI, 2020
Nyckelord
Aggregatibacter actinomycetemcomitans, Anti-citrullinated protein antibodies, leukotoxin A, rheumatoid arthritis
Nationell ämneskategori
Reumatologi och inflammation
Forskningsämne
reumatologi
Identifikatorer
urn:nbn:se:umu:diva-172727 (URN)10.3390/jcm9061906 (DOI)000553962800001 ()32570853 (PubMedID)2-s2.0-85114278889 (Scopus ID)
Tillgänglig från: 2020-06-23 Skapad: 2020-06-23 Senast uppdaterad: 2021-09-20Bibliografiskt granskad
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