Apical periodontitis and periodontal disease increase serum IL-17 levels in normoglycemic and diabetic rats

Cintra, Luciano Tavares Ângelo; Samuel, Renata Oliveira; Azuma, Mariane Maffei; Ribeiro, Clícia Pereira; Narciso, Luı́s; Lima, Valéria Marçal Felix de; Sumida, Dóris Hissako; Coclete, Gilberto Aparecido; Dezan, Elói; Gomes‐Filho, João Eduardo

doi:10.1007/s00784-014-1192-7

Cited by 49 publications

(90 citation statements)

References 31 publications

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“…The combination of PL and PD elevated the serum neutrophil levels in diabetic rats (Cintra et al . ). Another study demonstrated that diabetes mellitus upregulated IL‐17 production in PLs and elevated IL‐17 levels in hepatic and renal tissues of rats (Azuma et al .…”

Section: Review Of Identified Publicationsmentioning

confidence: 97%

The Presence and involvement of interleukin‐17 in apical periodontitis

2019

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Apical periodontitis (AP) is a chronic inflammatory disease characterized by periapical tissue inflammation and destruction of the associated alveolar bone. It is caused by microbial infections within the root canal and the resultant host immune responses in the periapical tissues. The proinflammatory cytokine interleukin (IL)‐17 has been shown to play an important role in many inflammatory diseases. There is increasing evidence of the presence of IL‐17 in AP, which might be associated with disease pathogenesis. Moreover, several animal studies indicate the potential role of IL‐17 in periapical inflammation and the resultant bone resorption in AP. This article reviews recent studies regarding the collective in vitro, in vivo and clinical evidence of the presence and involvement of IL‐17 in AP. A search related to IL‐17 in apical periodontitis was conducted on PubMed, EMBASE and Web of Science databases using keywords and controlled vocabulary. Two independent reviewers first screened titles and abstracts and then the full texts that were included. A total of 25 papers were identified, of the 25 included articles, 7 involved laboratory studies on cell cultures, 11 involved animal experimentations, and 7 were observational studies using human clinical samples. In conclusion, evidence for the presence of IL‐17 in AP from human and animal models is clear. However, there is relatively little information currently available that would highlight the specific role of IL‐17 in AP.

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Section: Review Of Identified Publicationsmentioning

confidence: 97%

The Presence and involvement of interleukin‐17 in apical periodontitis

2019

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“…Periodontitis is characterized by inflammation of the periodontal ligament and destruction of alveolar bone . Animal experiments and epidemiological researches confirm that severity of periodontitis is highly related to diabetes . Diabetes could cause complex systemic metabolic change in distant tissues, including periodontal ligament; and levels of inflammatory cytokines were elevated in periodontal tissue of diabetic patients .…”

Section: Introductionmentioning

confidence: 99%

The effect of NLRP inflammasome on the regulation of AGEs‐induced inflammatory response in human periodontal ligament cells

Zhang

et al. 2019

J of Periodontal Research

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Background and Objective Diabetes influences the frequency and development of periodontitis. Inflammation of human periodontal ligament cells (HPDLCs) participates in this pathologic process. Hence, this study aims to explore whether advanced glycation end products (AGEs), by‐products of diabetes, could exaggerate inflammation induced by muramyl dipeptide (MDP) in HPDLCs, and whether nucleotide‐binding oligomerization domain‐like receptors (NLRs) signaling pathway was involved. Material and Methods Human periodontal ligament cells were pre‐treated with 100 μg/mL AGEs for 24 hours and stimulated with 10 μg/mL MDP for 24 hours. IL‐6, IL‐1β, and RAGE were detected, and the activation of NF‐κB signaling pathway was observed. The expression of NLRs was evaluated with or without silencing RAGE or blocking NF‐κB pathway under AGEs stimulation. Statistical analyses were performed by using independent sample t test. Results Advanced glycation end products induced significant increase of inflammatory cytokines in HPDLCs (P < 0.05). Results of western blot (WB) showed that after 45 minutes stimulation of AGEs, p‐p65/p65 ratio peaked; AGEs promoted the expression of NLRP1, NLRP3, and apoptosis‐associated speck‐like protein containing a CARD (ASC). After silencing RAGE or blocking NF‐κB pathway, the up‐regulation of NLRs protein caused by AGEs was attenuated. Additionally, AGEs pre‐treatment could enhance the inflammatory response of MDP and the expression of NLRs, which were demonstrated by more expression of IL‐6, IL‐1β, NOD2, NLRP1, NLRP3, and ASC. Conclusion Advanced glycation end products induced inflammatory response in HPDLCs via NLRP1‐inflammasome and NLRP3‐inflammasome activation in which NF‐κB signal pathway was involved. Besides, AGEs promoted the inflammatory response of MDP via NOD2, NLRP1‐inflammasome, and NLRP3‐inflammasome.

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“…Inclui ainda deficiências em combate a infecções, devido a deficiências leucocitárias (26) , e reparos e/ou cicatrizações de processos patológicos, devido à isquemia vascular (6) . Na presente pesquisa, analisou-se, dentro de um banco de dados, a população de pacientes que apresentavam Diabetes Mellitus tipo II, geralmente diagnosticada em indivíduos com mais de 40 anos de idade, de ambos os sexos e obesos (80%).…”

Section: Discussionunclassified