The measurement of serum tumor necrosis factor-alpha levels in patients with lichen planus

Kara, Yeşim Akpınar

doi:10.4103/ijd.ijd_474_17

Cited by 7 publications

(5 citation statements)

References 15 publications

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“…Lymphocyte‐mediated immune response and locally released cytokines promote keratinocyte apoptosis. Consistently, human biopsies from OLP showed extensive epithelial layer destruction and numerous infiltrated lymphocytes, accompanied by high expression of the inflammatory cytokines TNF‐α and IL‐6, confirming previous reports (Kara, ; Mozaffari et al, ) and pointing to a role of these cytokines in the pathological process of OLP. The results of down‐regulated MASPIN and up‐regulated IKKα in OLP tissues attracted our attention.…”

Section: Discussionsupporting

confidence: 89%

“…Although the cause and pathogenesis of OLP remain unclear, previous studies have clarified that its aetiology includes stress, hypersensitivity, immune response, viral and bacterial infections (Cheng, Gould, Kurago, Fantasia, & Muller, ; Jaafari‐Ashkavandi, Mardani, Pardis, & Amanpour, ). Moreover, inflammatory cytokines play an important role in the pathogenesis of OLP, such as tumour necrosis factor‐alpha (TNF‐α), interleukin (IL‐6) and IL‐17 (Gueiros et al, ; Kara, ; Mozaffari, Sharifi, & Sadeghi, ).…”

Section: Introductionmentioning

confidence: 99%

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Role of mammary serine protease inhibitor on the inflammatory response in oral lichen planus

Liu

et al. 2019

Oral Diseases

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Objectives Oral lichen planus (OLP) is a chronic inflammatory condition with an unclear pathological mechanism. IκB kinase α (IKKα)‐regulated mammary serine protease inhibitor (MASPIN) has been shown to mediate inflammation, particularly in cancers. Here, we explored the expression of MASPIN in OLP and its role in the inflammatory response. Materials and Methods Immunohistochemistry staining and reverse transcription‐polymerase chain reaction assays were used to detect the subcellular localization and expression of MASPIN and IKKα in OLP and healthy control tissues. Levels of the inflammatory factors were compared with enzyme‐linked immunosorbent assays. MASPIN and IKKα were overexpressed and silenced, respectively, in an inflammation model of human oral keratinocytes (HOKs) stimulated with lipopolysaccharide (LPS). Results Mammary serine protease inhibitor expression was down‐regulated, whereas IKKα expression was up‐regulated in OLP tissues (p < 0.01). The levels of tumour necrosis factor‐alpha and interleukin‐6 in OLP tissues were increased compared to those of healthy controls (p < 0.01). MASPIN overexpression in LPS‐stimulated HOK cells inhibited the levels of IKKα and the secretion of inflammatory cytokines. By contrast, IKKα silencing promoted the expression of MASPIN and inhibited the secretion of inflammatory cytokines. Conclusion Both MASPIN and IKKα are involved in the inflammatory process of OLP, suggesting potential therapeutic targets.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Role of mammary serine protease inhibitor on the inflammatory response in oral lichen planus

Liu

et al. 2019

Oral Diseases

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“…In LP, TNF-α binding to tumor necrosis factor receptor-1 (TNFR-1) can promote apoptosis. 8 The increased release of TNF-α in LP damages the mucosa and interferes with the tissue repair program via induction of a soluble natural antagonist of IL-22, decreases the collagen content, aggregates with adhesion molecules (integrins, selectins, cadherins) and aggravates the inflammatory response. 9 , 10 Some researchers have found a correlation between TNF-α and the number of lymphocytes infiltrating LP lesions.…”

Section: Discussionmentioning

confidence: 99%

Expression and Significance of TNF-α and NF-κB/p65 in Cutaneous Lichen Planus

Chen¹,

Zhang²,

Sanjel³

et al. 2022

CCID

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Purpose The purpose of this study was to explore the expression of TNF-α and NF-κB/p65 in Lichen planus skin lesions and their correlation with the pathogenesis of Lichen planus. Patients and Methods The case group consisted of 30 individuals diagnosed with LP based on clinical and histopathologic examination. The control group consisted of 10 individuals from an Orthopedic Department with normal skin. TNF-α and NF-κB/p65 expression in skin tissue samples was detected by immunohistochemistry. Results The immunohistochemical results showed that TNF-α and NF-κB/p65 expression levels were significantly higher in LP skin lesions than normal skin tissues (P ≤ 0.05). Positive TNF-α staining mainly occurred in the cytoplasm of keratinocytes of the stratum granulosum, stratum spinosum, and stratum basale in the epidermis and lymphocytes in the superficial dermis. Positive NF-κB/p65 staining mainly occurred in the nucleus and cytoplasm of keratinocytes of the stratum spinosum and stratum basale in the epidermis and lymphocytes in the superficial dermis. Conclusion TNF-α and NF-κB/p65 are overexpressed in cutaneous LP. The two are positively correlated in LP, suggesting that they both play essential roles in the pathogenesis of LP.

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“…Apoptosis is central to the pathogenesis of lichen planus, as evidenced by cytotoxic T-cell infiltration into the epidermis, with subsequent secretion of tumor necrosis factor-alpha (TNF-α) and CD95 L (FasL) that are implicated in triggering the cascade of basal keratinocytes (KCs) apoptosis. [456]…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical expression of calmodulin in cutaneous lichen planus: A case–control study

et al. 2019

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Background: Calmodulin (CaM) is a multifunctional intermediate messenger protein that plays important role in cell motility, proliferation, and apoptosis. Therefore, it is thought to be involved in various ways in the apoptotic processes which are implicated in the pathogenesis of lichen planus. Objective: The aim of this study was to evaluate the immunohistochemical expression of CaM in lichen planus lesions in comparison to normal control skin to throw light on its possible role in disease pathogenesis. Patients and Methods: This case–control study was conducted on 50 patients with lichen planus, in addition to 20 age- and sex-matched healthy individuals. Skin biopsy specimens were taken from lesional skin of lichen planus patients as well as normal skin of controls. All were examined for immunohistochemical expression of CaM antibody. Results: There was statistically significant increase of the immunohistochemical expression of CaM in lesional skin of lichen planus patients compared with normal skin of controls (Chi-square test, P < 0.001). No significant correlation could be detected between CaM expression in lesional skin and the studied clinical parameters of lichen planus patients. Limitations: Tha main limitation of this study is its small sample size. Conclusion: CaM is upregulated in cutaneous lichen planus lesions suggesting a possible role in disease pathogenesis. Targeting CaM is expected to be a novel strategy for treatment of lichen planus.

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The measurement of serum tumor necrosis factor-alpha levels in patients with lichen planus

Cited by 7 publications

References 15 publications

Role of mammary serine protease inhibitor on the inflammatory response in oral lichen planus

Role of mammary serine protease inhibitor on the inflammatory response in oral lichen planus

Expression and Significance of TNF-α and NF-κB/p65 in Cutaneous Lichen Planus

Immunohistochemical expression of calmodulin in cutaneous lichen planus: A case–control study

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