TREM-1 Is Upregulated in Experimental Periodontitis, and Its Blockade Inhibits IL-17A and RANKL Expression and Suppresses Bone loss

Bostancı, Nagihan; Abe, Toshiharu; Belibasakis, Georgios N.; Hajishengallis, George

doi:10.3390/jcm8101579

Cited by 27 publications

(22 citation statements)

References 45 publications

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“…Several studies in experimental periodontitis suggest a pathogenic role for the Th17 subset. Genetic or pharmacologic inhibition of Th17 cells or IL-17 protects from periodontal bone loss, hence suggesting that these cells and their related pathways could potentially be exploited therapeutically (5,(67)(68)(69) (70). In this regard, patients with genetic defects in Th17 differentiation (due to loss-of-function STAT3 mutations) were shown to have reduced periodontal inflammation and bone loss compared to the general population (57).…”

Section: Il-17/th17 Host Responses In Oral Disease: Periodontal Disease and Candidiasis Il-17 In Periodontal (Gingival) Immunitymentioning

confidence: 99%

Regulation of host-microbe interactions at oral mucosal barriers by type 17 immunity

2020

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The oral mucosa is a primary barrier site and a portal for entry of microbes, food, and airborne particles into the gastrointestinal tract. Nonetheless, mucosal immunity at this barrier remains understudied compared with other anatomical barrier sites. Here, we review basic aspects of oral mucosal histology, the oral microbiome, and common and clinically significant diseases that present at oral mucosal barriers. We particularly focus on the role of interleukin-17 (IL-17)/T helper 17 (TH17) responses in protective immunity and inflammation in the oral mucosa. IL-17/TH17 responses are highly relevant to maintaining barrier integrity and preventing pathogenic infections by the oral commensal fungus Candida albicans. On the other hand, aberrant IL-17/TH17 responses are implicated in driving the pathogenesis of periodontitis and consequent bone and tooth loss. We discuss distinct IL-17–secreting T cell subsets, emphasizing their regulation and function in oropharyngeal candidiasis and periodontitis.

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Section: Il-17/th17 Host Responses In Oral Disease: Periodontal Disease and Candidiasis Il-17 In Periodontal (Gingival) Immunitymentioning

confidence: 99%

Regulation of host-microbe interactions at oral mucosal barriers by type 17 immunity

2020

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“…Furthermore, LP17 significantly downregulated the IL-17A and RANKL/OPG ratios. TREM-1 regulates the IL-17A-RANKL/OPG axis and bone loss in experimental periodontitis [53].…”

Section: Osteoclastsmentioning

confidence: 99%

Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease

Lin

Niimi

Ohsugi

et al. 2021

IJMS

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Periodontitis is an inflammatory disease characterized by the destruction of the periodontium. In the last decade, a new murine model of periodontitis has been widely used to simulate alveolar bone resorption and periodontal soft tissue destruction by ligation. Typically, 3-0 to 9-0 silks are selected for ligation around the molars in mice, and significant bone loss and inflammatory infiltration are observed within a week. The ligature-maintained period can vary according to specific aims. We reviewed the findings on the interaction of systemic diseases with periodontitis, periodontal tissue destruction, the immunological and bacteriological responses, and new treatments. In these studies, the activation of osteoclasts, upregulation of pro-inflammatory factors, and excessive immune response have been considered as major factors in periodontal disruption. Multiple genes identified in periodontal tissues partly reflect the complexity of the pathogenesis of periodontitis. The effects of novel treatment methods on periodontitis have also been evaluated in a ligature-induced periodontitis model in mice. This model cannot completely represent all aspects of periodontitis in humans but is considered an effective method for the exploration of its mechanisms. Through this review, we aimed to provide evidence and enlightenment for future studies planning to use this model.

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“…Periodontitis is a biofilm-driven chronic inflammatory disease during which a dysbiotic periodontal microbiota induces adverse immune responses that further lead to the destruction of tooth-supporting tissues and ultimately tooth loss [19][20][21] . Several studies have investigated TREM-1 and PGLYRP1 in the context of periodontal disease and recently TREM-1 has been suggested as a candidate marker for new treatment strategies against periodontal diseases 22,23 . Elevated TREM-1 levels were observed in saliva, serum and gingival crevicular fluids (GCF) in patients with periodontitis, and TREM-1 serum and saliva levels correlated positively [24][25][26][27] .…”

mentioning

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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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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TREM-1 Is Upregulated in Experimental Periodontitis, and Its Blockade Inhibits IL-17A and RANKL Expression and Suppresses Bone loss

Cited by 27 publications

References 45 publications

Regulation of host-microbe interactions at oral mucosal barriers by type 17 immunity

Regulation of host-microbe interactions at oral mucosal barriers by type 17 immunity

Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease

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

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