Upregulation of circulating inflammatory biomarkers under the influence of periodontal disease in rheumatoid arthritis patients

Panezai, Jeneen; Ali, A. A.; Ghaffar, Ambereen; Benchimol, Daniel; Altamash, Mohammad; Klinge, Björn; Engström, Per‐Erik; Larsson, Anders

doi:10.1016/j.cyto.2020.155117

Cited by 28 publications

(40 citation statements)

References 47 publications

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“…TREM-1 and PGLYRP1 levels in various biofluids are elevated in periodontitis patients compared to periodontally-healthy controls [24][25][26][27][28][29] . A recent study investigating 92 inflammatory biomarkers in serum of RA patients with and without periodontitis, identified 17 markers which were significantly elevated in serum of RA patients with periodontitis compared to periodontally-healthy RA patients 53 . The two inflammatory molecules investigated here, TREM-1 and PGLYRP1, followed the same trend.…”

Section: Discussionmentioning

confidence: 99%

Elevated serum TREM-1 is associated with periodontitis and disease activity in rheumatoid arthritis

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et al. 2021

Sci Rep

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The triggering receptor expressed on myeloid cells 1 (TREM-1) and peptidoglycan recognition protein 1 (PGLYRP1) are involved in the propagation of inflammatory responses. This study investigated whether serum levels of TREM-1 and PGLYRP1 correlate with periodontitis in rheumatoid arthritis (RA) patients. A total of 154 non-smoking participants with RA (n = 55, F/M: 41/14), Behçet´s disease (BD, n = 41, F/M: 30/11) and healthy controls (HC, n = 58, F/M: 40/18) were recruited. Serum and saliva were collected, the 28-joint disease activity score (DAS-28) was calculated and dental/periodontal measurements were recorded. Serum TREM-1 and PGLYRP1 levels were measured by ELISA and salivary bacterial DNA counts by quantitative polymerase chain reaction. TREM-1 and PGLYRP1 levels were higher in RA (166.3 ± 94.3; 155.5 ± 226.9 pg/ml) than BD (102.3 ± 42.8; 52.5 ± 26.3 pg/ml) and HCs (89.8 ± 55.7; 67.4 ± 37.3 pg/ml) (p < 0.05). In RA, periodontitis was associated with increased TREM-1 and PGLYRP1 levels (p < 0.05), yet in patients under methotrexate TREM-1 levels were lower. TREM-1 correlated with C-reactive protein (CRP) levels, DAS-28 and erythrocyte sedimentation rate, whereas PGLYRP1 positively correlated with CRP. RA patients displayed 3.5-fold higher salivary bacterial DNA counts than HCs. Increased serum TREM-1 levels correlated with PGLYRP1, CRP and DAS-28-ESR in RA patients with periodontitis.

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Section: Discussionmentioning

confidence: 99%

Elevated serum TREM-1 is associated with periodontitis and disease activity in rheumatoid arthritis

İnanç

Mumcu

Can

et al. 2021

Sci Rep

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“…For instance, higher IL-18 levels were found in serum but not in GCF from periodontitis patients with Crohn disease and ulcerative colitis compared with controls (Figueredo et al 2011). In addition, patients with RA and periodontitis had higher IL-18 levels in serum than patients with RA without periodontitis (Panezai et al 2020). Interestingly, initiation and progression of ligature-induced periodontitis in monkeys were characterized by a significant reduction of IL-18 mRNA levels in gingival samples (Ebersole et al 2014).…”

Section: Il-18mentioning

confidence: 99%

IL-1 Superfamily Members and Periodontal Diseases

et al. 2020

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Periodontitis is a complex, multifactorial chronic disease involving continuous interactions among bacteria, host immune/inflammatory responses, and modifying genetic and environmental factors. More than any other cytokine family, the interleukin (IL)–1 family includes key signaling molecules that trigger and perpetuate periodontal inflammation. Over the years, the IL-1 family expanded to include 11 members of cytokines, some with agonist activity (IL-1α, IL-1β, IL-18, IL-33, IL-36α, IL-36β, and IL-36γ), receptor antagonists (IL-1Ra, IL-36Ra), and 2 anti-inflammatory cytokines (IL-37, IL-38). The IL-1 receptor antagonist (IL-1Ra) has emerged as a pivotal player in the defense against periodontitis. IL-33 primarily induces the production of Th2-associated cytokines but acts as an “alarmin” via stimulation of mast cells. The IL-36 subclass of cytokines may be important in regulating mucosal inflammation and homeostasis. IL-37 suppresses innate and acquired immune responses. IL-38 is the most recent member of the IL-1 superfamily and has anti-inflammatory properties similar to those of IL-37 but through different receptors. However, limited evidence exists regarding the role of IL-37 and IL-38 in periodontitis. Despite the development of IL-1 blocking agents, therapeutic blockade of select IL-1 family members for periodontitis has only been partially investigated in preclinical and clinical research, while the development of IL-37 and IL-38 as novel anti-inflammatory drugs has not been considered adequately. Here, we review the key properties of the IL-1 family members and provide insights into targeting or promoting select cytokines as new therapeutic agents.

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“…The main source of soluble TWEAK in inflammatory tissue is macrophages / monocytes [15]. These data show that the TWEAK / Fn14 pathway makes significant contributions to inflammation in tissues and indicates that excessive or persistent upregulation of this pathway contributes significantly to the pathogenesis of some rheumatic inflammatory and infective diseases [16][17][18][19][20].…”

Section: Introductionmentioning

confidence: 76%