Interferon‐γ, Interleukins‐6 and ‐4, and Factor XIII‐A as Indirect Markers of the Classical and Alternative Macrophage Activation Pathways in Chronic Periodontitis

Navarrete, Mariely; García, J. E. Losa; Dutzan, Nicolás; Henríquez, Luis A.; Puente, Javier; Carvajal, Paola; Hernández, Marcela; Gamonal, Jorge

doi:10.1902/jop.2013.130078

Cited by 23 publications

(24 citation statements)

References 49 publications

(76 reference statements)

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“…However, there are conflicting reports regarding changes in the M2 phenotype 10,12,14,15 . Some studies found an enhancement of the M2 phenotype in periodontitis, 10 , 12 whereas other studies found a decrease 14 , 15 . In this context, phenotypic switch of macrophage M1/M2 remains uncertain because of the lack of an in situ analysis of the macrophage phenotypes using classic markers, including NOS2 and CD206 11 , 12 , 14 …”

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confidence: 99%

“…Clinical and animal studies that used either metabolic markers, 7–11 inflammatory cytokines, 11–13 or cell surface markers 11 , 14 for macrophage phenotyping, both in vivo and in vitro, have consistently suggested an enhanced phenotype and increase in the number of M1‐like macrophages in periodontitis. However, there are conflicting reports regarding changes in the M2 phenotype 10,12,14,15 . Some studies found an enhancement of the M2 phenotype in periodontitis, 10 , 12 whereas other studies found a decrease 14 , 15 .…”

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confidence: 99%

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Enhanced Activity of the Macrophage M1/M2 Phenotypes and Phenotypic Switch to M1 in Periodontal Infection

Takata

Zhao

Huang

et al. 2016

Journal of Periodontology

146

139

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confidence: 99%

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confidence: 99%

Enhanced Activity of the Macrophage M1/M2 Phenotypes and Phenotypic Switch to M1 in Periodontal Infection

Takata

Zhao

Huang

et al. 2016

Journal of Periodontology

146

139

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“…In IL-4, a proinflammatory cytokine is capable of inducing apoptosis of osteoblasts thus contributing to the progression of alveolar bone loss [9] and induces apoptosis in monocytes [17]; three polymorphisms (IL-4 −590 C/T (rs2243250), −33 C/T (rs2070874), and 70-bp) were addressed in a meta-analysis [17], which found, in most studies, no significant association between these genetic variants and the risk of developing periodontitis (Table 1). One of the possible explanations for such results is the potential publication that may have affected the evaluations for the 33-C/T and 70-pb polymorphisms because of the small number of studies for these polymorphisms (seven and four, resp.).…”

Section: Resultsmentioning

confidence: 99%

Genetic Factors and the Risk of Periodontitis Development: Findings from a Systematic Review Composed of 13 Studies of Meta-Analysis with 71,531 Participants

Silva

Carvalho

Alves

et al. 2017

International Journal of Dentistry

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Purpose. This work aimed to synthesize the results of recent meta-analysis focusing on polymorphism in inflammatory mediators and its relation with the risk of periodontitis development. Materials and Methods. A systematic search was conducted using databases for publications prior to October 2016. Three examiners extracted data from articles with a clear association between polymorphisms in the inflammatory mediator gene and the development of periodontitis through meta-analysis using the fixed or randomized statistical models to calculate the Odds Ratio with values of P < 0.05 considered significant. Results. A total of 13 meta-analysis articles with 25 polymorphisms in seven interleukins (IL-1A, IL-1B, IL-4, IL-6, IL-8, IL-10, and IL-18), three cellular receptors (Fcγ receptors: FCGR2A, FCGR3A, and FCGR3B), and five inflammatory mediators (COX-2, MMP-2, MMP-3, MMP-8, and MMP-9), with a total of 71,531 participants, approaching different classifications of the disease. Conclusion. The study demonstrated that polymorphisms in the IL-1A, IL-1B, IL-6, IL-10, MMP-3 (chronic form), and MMP-9 (chronic form) polymorphisms were significantly associated with the risk of developing periodontitis, whereas other polymorphisms in the IL-4, IL-8, IL-18, Fcγ, COX-2, MMP-2, MMP-3 (aggressive), MMP-8, and MMP-9 (aggressive) polymorphisms had no significant association with risk of developing periodontitis.

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“…Based on this result, we hypothesised that FXIII is involved in the activation of these cells. Recently, FXIII-A was reported to be a good marker of macrophage alternative pathway activation, but the interaction of coagulation factor FXIII with cells of the immune system has been demonstrated infrequently (Navarrete et al, 2014). This relationship includes the modification of FXIII expression during monocyte differentiation and monocyte-macrophage activation, and is supported by the presence of FXIII in the cytoplasm of monocytes/macrophages with phagocytic potential.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory cell populations in early neuroinflammation in the core and peri-ischemic lesions of rat brain after transient focal cerebral ischemia: A morphometric study

Horváth

Orădan

Chiriac

et al. 2018

Preprint

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Background and Objective:Clinical and experimental observations emphasize the role of inflammation as a direct risk factor for stroke. To better characterize the inflammation, we have conducted a detailed histological analysis of the inflammatory cell population after transient middle cerebral artery occlusion in a rat model. Methods:Fifteen adult Wistar male rats were divided randomly into test (n=10) and sham (n=5) groups. In the ischemic group, transient focal cerebral ischemia was induced with an intraluminal filament technique. Histologic lesions of the ischemic core and the surrounding penumbra zone were evaluated, based on a complex algorithm. Representative morphological changes in the core and the penumbra zone were compared. Immunohistochemistry was performed for leukocytes markers (CD15, CD68, CD3), leukocyte-released effectors (MMP-9 and COX-2), and FXIII (possibly involved in microglia and macrophage activation)Results: Neuronal vacuolation and degeneration were significantly more in the core lesion, whereas cellular edema and inflammatory infiltrate were increased in the penumbra. CD68, CD3, FXIII and Cox-2 expression were significantly higher in the penumbra than in the core (p=0.026; p=0.006; p=0.002; and p<0.001).Discussion: In the rat model of middle cerebral artery occlusion, inflammatory mechanisms, microglia/macrophage cells, and T-lymphocytes likely play an important role in the penumbra. The deterioration of neurons is less in the penumbra than in the core. Appreciation of the role of the inflammatory cells and mechanisms involved in stroke might lead to measures to inhibit the injury and save brain volume. ABSTRACT Background and Objective: Clinical and experimental observations emphasize the role of inflammation as a direct risk factor for stroke. To better characterize the inflammation, we have conducted a detailed histological analysis of the inflammatory cell population after transient middle cerebral artery occlusion in a rat model.

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Interferon‐γ, Interleukins‐6 and ‐4, and Factor XIII‐A as Indirect Markers of the Classical and Alternative Macrophage Activation Pathways in Chronic Periodontitis

Abstract: The presence of IFN-γ, IL-6, IL-4, and FXIII-A in healthy individuals and in patients with CP suggests that macrophages may be activated by both classic and alternative pathways in health and in periodontal disease.

Cited by 23 publications

References 49 publications

Enhanced Activity of the Macrophage M1/M2 Phenotypes and Phenotypic Switch to M1 in Periodontal Infection

Enhanced Activity of the Macrophage M1/M2 Phenotypes and Phenotypic Switch to M1 in Periodontal Infection

Genetic Factors and the Risk of Periodontitis Development: Findings from a Systematic Review Composed of 13 Studies of Meta-Analysis with 71,531 Participants

Inflammatory cell populations in early neuroinflammation in the core and peri-ischemic lesions of rat brain after transient focal cerebral ischemia: A morphometric study

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