Inflammation

Steinhoff, Martin; Groves, Richard; LeBoit, Philip E.; Luger, Thomas A.

doi:10.1002/9781444317633.ch12

Cited by 3 publications

(2 citation statements)

References 848 publications

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“…Therefore, the big question to be raised is why these patients were immune to such skin diseases. It is difficult to explain, but we can speculate that patients with pemphigus vulgaris secrete T-helper 1 and 2 cytokines in the sera, and lesional and perilesional skin, such as tumor necrosis alpha, interleukin 6 and 1a, and interferon c. [18][19][20][21][22] These cytokines might act as a defense mechanism against infections and tumors. To the best of our knowledge, this is the first study that concluded this new hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Skin tumors and skin infections in kidney transplant recipients vs. patients with pemphigus vulgaris

2013

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Section: Discussionmentioning

confidence: 99%

Skin tumors and skin infections in kidney transplant recipients vs. patients with pemphigus vulgaris

2013

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“…Normally, COX-2 expression is not detectable or is very low, but it generally increases with pain and inflammation [ 8 ]. COX-2 protein was detected in the perinuclear region of normal cells [ 9 ] and in the cytoplasm of tumor cells, particularly in the perinuclear membranes of keratinocytes [ 10 ]. In some studies, non-steroidal anti-inflammatory drugs (NSAIDs) have been reported to inhibit carcinogenesis in humans and rodents.…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical Analysis of Cyclooxygenase-2 in Non-Melanocytic Skin Cancer: Correlation With Morphological Subtype and Histologic Grade

Koyuncuer

2014

World J Oncol

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BackgroundBasal cell carcinomas (BCCs) and squamous cell carcinomas (SCCs) are known as non-melanoma skin cancers (NMSCs), and they account for approximately 90% of all skin cancers. Cyclooxygenase-2 (COX-2) is expressed in NMSC and in premalignant cutaneous lesions (actinic keratosis).MethodsImmunohistochemistry was performed with COX-2 antibodies in skin biopsies (paraffin tissue archival blocks) from 28 cases with SCC and 33 cases with BCC.ResultsCOX-2 was immunostained in a total of 61 cases. There was no staining or weakly positive staining in 73.8% of the cases (45 cases), and there was moderate or strong positive staining in 26.3% of the cases (16 cases). COX-2 was expressed in 42.4% of the BCC cases and in 57.1% of the SCC cases. There was a significant relationship between positive COX-2 staining and SCC (P = 0.016).ConclusionsIn this study, SCCs were significantly correlated with the expression of COX-2. In addition, COX-2 was more frequently expressed in SCC than in BCC. The largest diameters of the SCC were significantly correlated with the expression of COX-2. There were no significant associations between COX-2 staining and clinicopathologic features such as the ulceration of the tumor, its anatomic localization, patient gender, the histologic grade of the SCC and the morphological subtype of the BCC.

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Capsaicin attenuates the effect of inflammatory cytokines in a HaCaT cell model for basal keratinocytes

Cervantes Recalde,

Schmidt,

Girardi

et al. 2024

Front. Pharmacol.

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IntroductionThe resolution of the skin’s inflammatory response is only possible if its barrier function is restored. TRPV1 channel activation plays an important role during inflammation but the effect of this activation on the skin barrier under inflammatory conditions has not been clarified. We hypothesize that it could potentially aid the keratinocyte barrier by reducing inflammatory cytokine release and promoting tight junction development.MethodsTo explore the role of TRPV1 activation in inflammation, we designed and optimized an in vitro model of keratinocytes with basal epidermal layer characteristics using HaCaT cells and TNFα to induce inflammation.ResultsTNFα increased the gene expression of tight junction protein claudin 1 (CLDN1) by at least 2.60 ± 0.16-fold, in a concentration-dependent manner, over a 48 h period. The administration of a capsaicin pre-treatment reduced the CLDN1 expression to 1.51 ± 0.16-fold during the first 6 h after TNFα induction, whereas IL-8 cytokine release was reduced 0.64 ± 0.17-fold. After 48 h, CLDN1 protein levels increased by a factor of 6.57 ± 1.39 compared to cells only treated with TNFα.DiscussionThese results suggest that activation of TRPV1 by capsaicin can potentiate the increase in CLDN1 expression and CLDN1 protein synthesis induced by TNFα in cultured keratinocytes, while reducing the release of IL-8.

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Inflammation

Cited by 3 publications

References 848 publications

Skin tumors and skin infections in kidney transplant recipients vs. patients with pemphigus vulgaris

Skin tumors and skin infections in kidney transplant recipients vs. patients with pemphigus vulgaris

Immunohistochemical Analysis of Cyclooxygenase-2 in Non-Melanocytic Skin Cancer: Correlation With Morphological Subtype and Histologic Grade

Capsaicin attenuates the effect of inflammatory cytokines in a HaCaT cell model for basal keratinocytes

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