Gingival Concentrations of Interleukin‐23 and ‐17 at Healthy Sites and at Sites of Clinical Attachment Loss

Lester, S. Reid; Bain, Jennifer; Johnson, Roger B.; Serio, Francis G.

doi:10.1902/jop.2007.060458

Cited by 102 publications

(86 citation statements)

References 48 publications

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“…4 In relation to chronic periodontitis, a significant elevation of the total amount of IL-17 had been demonstrated in the gingival crevicular fluid samples and culture supernatants of gingival cells in periodontitis patients compared to healthy controls that suggested a role for IL-17 in the pathogenesis of chronic periodontitis. 5 The involvement of IL-17 in the host response of periodontal disease is further supported by Lester et al 6 , who reported an increased concentration of IL-17 in gingival tissue supernatants at sites with moderate to severe CAL and had found a positive correlation between them at the site-based level.…”

Section: Introductionmentioning

confidence: 84%

Serum interleukin-17 (IL-17) in chronic periodontitis patients

et al. 2017

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Introduction: Explorations into the periodontal medicine relationship have discovered interleukin-17 (IL-17) cytokine as one of the pro-inflammatory mediators that play a crucial role in the initiation and progression of the chronic periodontal disease. This case and control study aimed to compare the serum IL-17 concentration between chronic periodontitis and healthy subjects and to assess the relationship between the IL-17 serum and the clinical periodontal parameters in chronic periodontitis patients. Methods: This study was a case-control study. The subjects were selected using purposive sampling method. The periodontal screening assessment in the Family Treatment Center and Postgraduate Dental Clinic, Universiti Sains Malaysia Hospital. A total of 55 samples who fit with the inclusion and exclusion study criteria of full-mouth clinical periodontal records together with blood serums were obtained from 28 chronic periodontitis patients and from 27 healthy subjects. The concentration of IL-17 cytokine in serum was measured using ELISA test. Results: Subjects with periodontal disease presented significantly worse clinical parameters (p<0.001) compared to control. The level of serum IL-17 concentration was significantly higher (p=0.026) in chronic periodontitis subjects 3.6 (1.03) pg/mL compared to the control 3.1 (0.70) pg/mL. Conclusions: There was no correlation between the level of IL-17 concentration in the serum and clinical periodontal parameters.

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Section: Introductionmentioning

confidence: 84%

Serum interleukin-17 (IL-17) in chronic periodontitis patients

et al. 2017

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“…Importantly, increased P. gingivalis-induced expression of heterodimeric IL-23, composed of p40 and p19, and connected to Th17 survival, were consistent with pro-inflammatory IL-17 ϩ cells within the lesions and inflamed gingiva. 58 IL-17 in turn accelerates innate cell recruitment and activation through IL-8, CXCL1, TNF, GM-CSF, and facilitates osteoclastogenesis. 59 One of the hallmarks and most devastating aspects of periodontal disease is the destruction to the supporting structures of the tooth, involving osteoclastogenesis and bone resorption.…”

Section: Discussionmentioning

confidence: 99%

Rapid Myeloid Cell Transcriptional and Proteomic Responses to Periodontopathogenic Porphyromonas gingivalis

Nares

Moutsopoulos

Angelov

et al. 2009

The American Journal of Pathology

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Long-lived monocytes, macrophages, and dendritic cells (DCs) are Toll-like receptor-expressing, antigenpresenting cells derived from a common myeloid lineage that play key roles in innate and adaptive immune responses. Based on immunohistochemical and molecular analyses of inflamed tissues from patients with chronic destructive periodontal disease, these cells, found in the inflammatory infiltrate, may drive the progressive periodontal pathogenesis. To investigate early transcriptional signatures and subsequent proteomic responses to the periodontal pathogen, Porphyromonas gingivalis, donor-matched human blood monocytes, differentiated DCs, and macrophages were exposed to P. gingivalis lipopolysaccharide (LPS) and gene expression levels were measured by oligonucleotide microarrays. In addition to striking differences in constitutive transcriptional profiles between these myeloid populations, we identify a P. gingivalis LPS-inducible convergent, transcriptional core response of more than 400 annotated genes/ESTs among these populations, reflected by a shared, but quantitatively distinct, proteomic response. Nonetheless, clear differences emerged between the monocytes, DCs, and macrophages. The finding that long-lived myeloid inflammatory cells, particularly DCs, rapidly and aggressively respond to P. gingivalis LPS by generating chemokines, proteases, and cytokines capable of driving T-helper cell lineage polarization without evidence of corresponding immunosuppressive pathways highlights their prominent role in host defense and progressive tissue pathogenesis. The shared, unique, and/or complementary transcriptional and proteomic profiles may frame the context of the host response to P. gingivalis, contributing to the destructive nature of periodontal inflammation.

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“…Our findings are thus consistent with the elevated levels of IL-17 in human periodontitis [4,[93][94][95] and in mouse periodontitis models [74,96]. IL-17 was also shown to stimulate antimicrobial immunity and thereby to inhibit pathogen-initiated bone loss in a relatively acute periodontitis model [97];…”

Section: Resultssupporting

confidence: 88%

“…To our knowledge, the abrogation of periodontitis in Oel-r / --IL-17R- [4,[93][94][95] and in mouse periodontitis models [74,96]. IL-17…”

Section: Discussionmentioning

confidence: 99%

Age-associated changes in innate immunity and their impacts on inflammatory disease.

Eskan¹

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Gingival Concentrations of Interleukin‐23 and ‐17 at Healthy Sites and at Sites of Clinical Attachment Loss

Abstract: Our results suggested the possibility that the IL-23/IL-17 immune response was present within chronically inflamed gingiva. This is a host response that had not been reported previously in periodontal disease and may be an important factor in the chronic nature of the disease.

Cited by 102 publications

References 48 publications

Serum interleukin-17 (IL-17) in chronic periodontitis patients

Serum interleukin-17 (IL-17) in chronic periodontitis patients

Rapid Myeloid Cell Transcriptional and Proteomic Responses to Periodontopathogenic Porphyromonas gingivalis

Age-associated changes in innate immunity and their impacts on inflammatory disease.

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