Tumor Necrosis Factor‐α Inhibits Transforming Growth Factor‐β–Stimulated Myofibroblastic Differentiation and Extracellular Matrix Production in Human Gingival Fibroblasts

Arancibia, Rodrigo; Oyarzún, Alejandro; Silva, Daniel; Tobar, Nicolás; Martı́nez, Jorge; Ph, Smith

doi:10.1902/jop.2012.120225

Cited by 33 publications

(33 citation statements)

References 48 publications

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“…[8] TNF-α was reported to downregulate the production of tissue growth factor-β1, which in turn could stimulate extracellular matrix molecules. [9] It has long been known that TNFα could inhibit the synthesis of type I, III collagen, and fibronectin. [10] It was reported [11] that T helper cell 17 cells inhibited collagen production with a mechanism partially dependent on interleukin-17, TNF, and interferon-γ.…”

Section: Discussionmentioning

confidence: 99%

Successful treatment of infliximab in a patient with scleroderma

Liu²,

Xu³

2017

Medicine

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Rationale:Systemic Scleroderma (SSc) is a rare connective tissue disease clinically characterized by cutaneous sclerosis and variable systemic involvement. No drug is currently available to effectively reverse the fibrotic process in SSc. Previous reports have suggested that the tumor necrosis factor (TNF) antagonists could be useful for the treatment of fibrotic disorders. However, TNFα has long been considered as an antifibrotic cytokine. Whether TNF antagonist is effective for SSc patients needs to be tested.Patient concerns-Diagnosis:Here we report a case with a 2-year history of SSc who was effectively treated with infliximab in our clinic.Interventions:The patient manifested skin thickening, chest tightness and arthralgia. Before admitted to our clinic, he was treated with methylprednisolone, prostacyclin, D-penicillamine and calcium antagonists but without significant improvement of his signs and symptoms. In our clinic, the patient was treated with infliximab.Outcomes:His signs and symptoms were continued improving during the course of treatment. His skin biopsy showed significant reduction in fibroplasia finally.Lessons:TNF antagonist is an effective treatment for SSc.

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Section: Discussionmentioning

confidence: 99%

Successful treatment of infliximab in a patient with scleroderma

Liu²,

Xu³

2017

Medicine

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“…All of these studies suggest that infiltration by inflammatory cells seems to be critical for the prevention of an infection. However, a prolonged inflammatory response may delay wound healing and probably favor tissue fibrosis, reducing the chances of true regeneration (Pacios et al 2012;Arancibia et al 2013). It is important to consider that several studies have documented that aging cells and tissues show increased levels of inflammation (Chung et al 2011).…”

Section: The Inflammatory Phase Of Wound Healingmentioning

confidence: 99%

Gingival Wound Healing

Cáceres

Martínez

et al. 2014

J Dent Res

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Gingival wound healing comprises a series of sequential responses that allow the closure of breaches in the masticatory mucosa. This process is of critical importance to prevent the invasion of microbes or other agents into tissues, avoiding the establishment of a chronic infection. Wound healing may also play an important role during cell and tissue reaction to long-term injury, as it may occur during inflammatory responses and cancer. Recent experimental data have shown that gingival wound healing is severely affected by the aging process. These defects may alter distinct phases of the wound-healing process, including epithelial migration, granulation tissue formation, and tissue remodeling. The cellular and molecular defects that may explain these deficiencies include several biological responses such as an increased inflammatory response, altered integrin signaling, reduced growth factor activity, decreased cell proliferation, diminished angiogenesis, reduced collagen synthesis, augmented collagen remodeling, and deterioration of the proliferative and differentiation potential of stem cells. In this review, we explore the cellular and molecular basis of these defects and their possible clinical implications.

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“…Junto a estos fibroblastos y otras células de defensa, se producen citocinas pro-inflamatorias (Ara et al 2013, Baek et al 2013) como la Interleucina 1ß (IL 1ß; Bhawal et al 2012, Sawada et al 2013, Factor de Necrosis Tumoral alfa (TNFα; Guimarães et al 2011, Arancibia et al 2013) y citocinas anti-inflamatorias como lainterleucina10 (IL-10); que controla una respuesta inflamatoria exacerbada (Morandini et al 2011, Gómez-Florit et al 2013. De esta forma, la regulación de las funciones de remodelación del tejido conectivo y respuesta inflamatoria de los fibroblastos gingivales con medicamentos antihomotóxicos, podría tener un gran potencial terapéutico en periodoncia (Saini et al 2012).…”

Section: Medición De La Citotoxicidad Y Producción De Citocinas En Fiunclassified

Medición de la citotoxicidad y producción de citocinas en fibroblastos gingivales humanos estimulados con Mercurius−Heel®S: Un estudio piloto

Robayo

Patiño²,

Rueda³

2014

Univ. Sci.

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Mercurius-Heel®S is a homeopathic remedy used to treat infectious diseases such as gingivitis and periodontitis, mainly in the oral cavity. The main component of this drug is the Mercurius solubilis. Its cytotoxic effect was established based on cell viability and its anti-inflammatory effect by measuring the cytokines Mercurius-Heel®S on human gingival fibroblasts (FGH). We treated cells with Mercurius-Heel®S at concentrations of 300 mg/ml to 0.0005 mg/ml and left untreated cells as a control. Cell viability was measured using the MTS® colorimetric assay and the expression of cytokines (IL1b, TNFa e IL10) present in cell supernatants was performed with Quantiquine® ELISA. From 3.7 mg/ml to 0.0005 mg/ml, we observed a significantly higher increase in cell viability in comparison to the control (lower concentrations of the drug). Cytokine production was not significantly different at different concentrations of Mercurius-Heel®S. There was no significant increase in IL1b, IL10 and TNFa and Mercurius-Heel®S showed no cytotoxic effect on FGH.

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Tumor Necrosis Factor‐α Inhibits Transforming Growth Factor‐β–Stimulated Myofibroblastic Differentiation and Extracellular Matrix Production in Human Gingival Fibroblasts

Cited by 33 publications

References 48 publications

Successful treatment of infliximab in a patient with scleroderma

Successful treatment of infliximab in a patient with scleroderma

Gingival Wound Healing

Medición de la citotoxicidad y producción de citocinas en fibroblastos gingivales humanos estimulados con Mercurius−Heel®S: Un estudio piloto

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