Activation of nuclear factor‐kappa B correlates with tumor necrosis factor‐alpha in oral lichen planus: a clinicopathologic study in atrophic‐erosive and reticular form

Zhou, Gang; Xia, Kun; Du, Ge-Fei; Chen, Xinming; Xu, Xue-yi; Li, Rui; Zhou, Hongmei

doi:10.1111/j.1600-0714.2009.00779.x

Cited by 58 publications

(37 citation statements)

References 25 publications

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“…Such an approach has been employed previously in clinicopathologic studies [20-22] to assess the potential for p65 transactivation based on its cytoplasmic-to-nuclear translocation within tissue specimens, including fetal membranes [23]. …”

Section: Resultsmentioning

confidence: 99%

Nuclear factor-kappa B localization and function within intrauterine tissues from term and preterm labor and cultured fetal membranes

Vora

Abbas

Kim

et al. 2010

Reprod Biol Endocrinol

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BackgroundThe objective of this study was to quantify the nuclear localization and DNA binding activity of p65, the major transactivating nuclear factor-kappa B (NF-kappaB) subunit, in full-thickness fetal membranes (FM) and myometrium in the absence or presence of term or preterm labor.MethodsPaired full-thickness FM and myometrial samples were collected from women in the following cohorts: preterm no labor (PNL, N = 22), spontaneous preterm labor (PTL, N = 21), term no labor (TNL, N = 23), and spontaneous term labor (STL, N = 21). NF-kappaB p65 localization was assessed by immunohistochemistry, and DNA binding activity was evaluated using an enzyme-linked immunosorbent assay (ELISA)-based method.ResultsNuclear p65 labeling was rare in amnion and chorion, irrespective of clinical context. In decidua, nuclear p65 labeling was greater in the STL group relative to the TNL cohort, but there were no differences among the TNL, PTL, and PNL cohorts. In myometrium, diffuse p65 nuclear labeling was significantly associated with both term and preterm labor. There were no significant differences in ELISA-based p65 binding activity in amnion, choriodecidual, and myometrial specimens in the absence or presence of term labor. However, parallel experiments using cultured term fetal membranes demonstrated high levels of p65-like binding even the absence of cytokine stimulation, suggesting that this assay may be of limited value when applied to tissue specimens.ConclusionsThese results suggest that the decidua is an important site of NF-kappaB regulation in fetal membranes, and that mechanisms other than cytoplasmic sequestration may limit NF-kappaB activation prior to term.

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Section: Resultsmentioning

confidence: 99%

Nuclear factor-kappa B localization and function within intrauterine tissues from term and preterm labor and cultured fetal membranes

Vora

Abbas

Kim

et al. 2010

Reprod Biol Endocrinol

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“…OLP is associated with an increased risk of malignant transformation [5]. Increased expressions of nuclear factor kappa B (NF-jB) signalling molecules and various inflammatory cytokines such as tumour necrosis factor (TNF)-a and interleukin (IL)-1b have been demonstrated previously in OLP [7][8][9]. Increased expressions of nuclear factor kappa B (NF-jB) signalling molecules and various inflammatory cytokines such as tumour necrosis factor (TNF)-a and interleukin (IL)-1b have been demonstrated previously in OLP [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

New evidence of connections between increased O-GlcNAcylation and inflammasome in the oral mucosa of patients with oral lichen planus

Thi

Phoomak

Champattanachai

et al. 2018

Clinical and Experimental Immunology

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Oral lichen planus (OLP) is considered a chronic inflammatory immune-mediated disease of the oral mucosa. Immunopathogenesis of OLP is thought to be associated with cell-mediated immune dysregulation. O-GlcNAcylation is a form of reversible glycosylation. It has been demonstrated that O-GlcNAcylation promoted nuclear factor kappa B (NF-κB) signalling. Activation of NF-кB can induce expression of nucleotide-binding domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, which is a large intracellular multi-protein complex involving an immune response. Dysregulated expression of the NLRP3 inflammasome was reported to be associated with autoinflammatory diseases. No integrative studies between O-GlcNAcylation and NLRP3 inflammasome in OLP patients have been reported. The present study aimed to determine the immunohistochemical expression of O-GlcNAcylation, NF-κB signalling molecules and NLRP3 inflammasome in oral mucosae of OLP patients. Oral tissue samples were collected from 30 OLP patients and 30 healthy individuals. Immunohistochemical staining and analyses of immunostaining scores were performed to evaluate expression of O-GlcNAcylation, NF-κB signalling molecules and NLRP3 inflammasome. According to observations in this study, significantly higher levels of O-GlcNAcylation, NF-κB signalling molecules and NLRP3 inflammasome were demonstrated in OLP patients compared with control subjects (P < 0·001). Positive correlations among O-GlcNAcylation, NF-κB signalling molecules and NLRP3 inflammasome were also observed in OLP samples (P < 0·01). In conclusion, the present study provides supportive evidence that increased O-GlcNAcylation is associated with increased expression of NLRP3 inflammasome via the NF-κB signalling pathway. These findings provide a new perspective on immunopathogenesis of OLP in relation to autoinflammation.

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“…On the contrary, we have paradoxically recorded quasi-significant values (p=0.05) observing the PFn level variations in reticular OLP patients in whom there are no chronic wounds. These unexpected data could reflect the differences observed in epithelial activity, apoptosis and peripheral immunocompetent cells in reticular and atrophic-erosive OLP (15)(16)(17)(18).…”

Section: Discussionmentioning

confidence: 98%

Analysis of Plasma Fibronectin Levels in Patients Affected by Oral Lichen Planus

et al. 2012

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Previous studies have demonstrated that patients affected by Oral Lichen Plauns (OLP) show lower levels of salivary fibronectin when compared with normal controls. Similarly, tissutal fibronectin expression is lost in epidermal basal layer and papillary dermis of OLP patients. To date, no data exist on the potential role of Plasma Fibronectin(PFn) in OLP pathogenesis, diagnosis and treatment. The objectives ofthe present study are: a) to determine the PFn levels in OLP patients; b) to evaluate a possible association between OLP clinical form and PFn levels; and c) to determine the PFn levels in relation to OLP signs and symptoms treatment. Twenty consecutive patients affected by OLP were enrolled. All patients were treated for eight weeks with topical c1obetasol 0.05%. OLP signs and symptoms were scored before and after treatment. PFn level was determined by a nephelometric system. OLP signs and symptoms significantly improved after treatment. The mean levels of PFn were 31.84mg/dL at the beginning and 26.76mg/dL at the end of the study. The difference was not statistically significant (p=0.60). PFn in OLP patients remains in normal value range. OLP clinical form does not influence the PFn levels. Amelioration of symptoms and signs of atrophic-erosive and reticular OLP are induced by c1obetasol treatment and the PFn seems not to interfere in the healing processes induced by topical corticosteroid. In contrast to what is observed in traumatic or diabetic wound healing, levels of PFn do not promote OLP lesion healing. PFn is not to be considered as a marker of OLP disease activity and its role in OLP pathogenesis still remains unclear.Two major forms of fibronectin are produced and secreted by human cells in vitro and in vivo (l). The cell-associated fibronectin is relatively insoluble and supports cell adhesion, wound healing, cell differentiation and phagocytosis. The plasma fibronectin (PFn), produced primarily in the liver, is a soluble serum protein with biological properties similar to those of cell fibronectin. It mediates a variety of cellular interactions with the extracellular matrix and plays important roles in cell adhesion, migration, growth and differentiation (2).Oral lichen planus (aLP) is aT-cell-mediated autoimmune disease but its cause is still unknown. Activated T cells are attracted and migrate towards the oral epithelium (homing), as the result of intercellular adhesion molecules (ICAM-I and

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Activation of nuclear factor‐kappa B correlates with tumor necrosis factor‐alpha in oral lichen planus: a clinicopathologic study in atrophic‐erosive and reticular form

Cited by 58 publications

References 25 publications

Nuclear factor-kappa B localization and function within intrauterine tissues from term and preterm labor and cultured fetal membranes

Nuclear factor-kappa B localization and function within intrauterine tissues from term and preterm labor and cultured fetal membranes

New evidence of connections between increased O-GlcNAcylation and inflammasome in the oral mucosa of patients with oral lichen planus

Analysis of Plasma Fibronectin Levels in Patients Affected by Oral Lichen Planus

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