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»Gönnen Sie Ihrer Haut Zukunft.« Unter diesem Slogan wirbt die Frankfurter Oberbürgermeisterin Petra Roth als Schirmherrin der Deutschen Hautkrebsstiftung (www.hautkrebsstiftung.de) für Maßnahmen zur Prävention von Hauttumoren. Diese Krebsformen nehmen derzeit weltweit in der hellhäutigen Bevölkerung am stärksten zu, wobei aufgrund unserer bereits in frühen Jahren sonnenbelasteten Freizeitgewohnheiten mehr und mehr jüngere Menschen erkranken. Neue Therapieoptionen erlauben es, Krebs sowie Krebsvorstufen früher und effektiver zu behandeln. Dabei spielen insbesondere nichtinvasive Methoden eine immer wichtigere Rolle. Cremen statt schneiden – dies ist nicht immer, aber immer öfter die richtige Lösung.
Background: Bacterial meningitis is associated with high mortality and long-term neurological sequelae. Increasing the phagocytic activity of microglia could improve the resistance of the CNS against infections. We studied the influence of activin A, a member of the TGF-β family with known immunoregulatory and neuroprotective effects, on the functions of microglial cells in vitro.
Methods: Primary murine microglial cells were treated with activin A (0.13 ng/ml–13 μg/ml) alone or in combination with agonists of TLR2, 4, and 9. Phagocytosis of Escherichia coli K1 as well as release of TNF-α, IL-6, CXCL1, and NO was assessed.
Results: Activin A dose-dependently enhanced the phagocytosis of Escherichia coli K1 by microglial cells activated by agonists of TLR2, 4, and 9 without further increasing NO and proinflammatory cytokine release. Cell viability of microglial cells was not affected by activin A.
Conclusions: Priming of microglial cells with activin A could increase the elimination of bacteria in bacterial CNS infections. This preventive strategy could improve the resistance of the brain to infections, particularly in elderly and immunocompromised patients.
Psoriasis is a frequent and often severe inflammatory skin disease, characterized by altered epidermal homeostasis. Since we found previously that Akt/mTOR signaling is hyperactivated in psoriatic skin, we aimed at elucidating the role of aberrant mTORC1 signaling in this disease. We found that under healthy conditions mTOR signaling was shut off when keratinocytes switch from proliferation to terminal differentiation. Inflammatory cytokines (IL-1β, IL-17A, TNF-α) induced aberrant mTOR activity which led to enhanced proliferation and reduced expression of differentiation markers. Conversely, regular differentiation could be restored if mTORC1 signaling was blocked. In mice, activation of mTOR through the agonist MHY1485 also led to aberrant epidermal organization and involucrin distribution. In summary, these results not only identify mTORC1 as an important signal integrator pivotal for the cells fate to either proliferate or differentiate, but emphasize the role of inflammation-dependent mTOR activation as a psoriatic pathomechanism.
Fragestellung Intoleranzreaktionen auf nicht-steroidale Antiphlogistika sind häufig und basieren auf der Hemmung des Enzyms Cyclooxygenase-1 (COX-1), wohingegen deren therapeutische Effekte auf einer COX-2 Hemmung beruhen. In dieser Studie wurde die Verträglichkeit des selektiven COX-2 Inhibitors Celecoxib bei Patienten mit Intoleranzreaktionen auf nicht-steroidale Antiphlogistika untersucht. Methodik Bei 77 Patienten (24 Männer, 53 Frauen) mit Intoleranzreaktionen auf nicht-steroidale Antiphlogistika wurden standardisierte Hauttestungen (Prick, Scratch, Epikutantestung) sowie anschließend orale fraktionierte Placebo-kontrollierte einfach blinde Expositionstestungen unter Einschluß von Celecoxib (maximale Einzeldosis 200mg, kumukative Tagesdosis 350mg) durchgeführt. Ergebnisse 21 Patienten wiesen anamnestisch lediglich Hautsymptome (Urtikaria) auf, 25 Patienten nur eine Atemwegssymptomatik (Asthma), bei 18 Patienten traten Haut- und Atemwegssymptome auf, und bei 13 Patienten war es zu einem anaphylaktischen Schock gekommen. Azetylsalizylsäure war in 38 Fällen ein Auslöser der Beschwerden. In 46 Fällen verursachten mehrere nicht-steroidale Antiphlogistika chemisch unterschiedlicher Gruppen die Symptomatik. Die orale Expositionstestung mit Celecoxib verlief bei allen 77 Patienten unauffällig. Schlußfolgerung Vor dem Hintergrund der hohen Inzidenz von Intoleranzreaktionen gegen nicht-steroidale Antiphlogistika stellt der Einsatz selektiver COX-2 Inhibitoren eine therapeutische Alternative sowie eine geeignete Maßnahme zur Prävention entsprechender Reaktionen dar.
Preserving a patient’s own teeth—even in a difficult situation—is nowadays preferable to surgical intervention and therefore promotes development of suitable dental repair materials. Biodentine®, a mineral trioxide aggregate substitute, has been used to replace dentine in a bioactive and biocompatible manner in both the dental crown and the root. The aim of our study was to evaluate the influence of Biodentine® on pulp fibroblasts in vitro. For this study, one to five Biodentine® discs with a diameter of 5.1mm were incubated in DMEM. To obtain Biodentine® suspensions the media were collected and replaced with fresh medium every 24h for 4 days. Primary pulp cells were isolated from freshly extracted wisdom teeth of 20–23 year old patients and incubated with the Biodentine® suspensions. Proliferation, cell morphology, cell integrity and cell viability were monitored. To evaluate the effect of Biodentine® on collagen type I synthesis, the secretion of the N-terminal domain of pro-collagen type I (P1NP) and the release of transforming growth factor-β1 (TGF-β1) were quantified. None of the Biodentine® suspensions tested influenced cell morphology, proliferation or cell integrity. The cell viability varied slightly depending on the suspension used. However, the concentrations of P1NP of all pulp fibroblast cultures treated for 24h with the moderate to high Biodentine® concentration containing suspensions of day 1 were reduced to 5% of the control. Furthermore, a significant TGF-β1 reduction was observed after treatment with these suspensions. It could be shown that Biodentine® is biocompatible. However, dissolved particles of the moderate to high concentrated Biodentine® suspensions 24h after mixing induce a significant reduction of TGF-β1 release and reduce the secretion of collagen type I of primary pulp fibroblasts.
High tumor interstitial fluid pressure (TIFP) is a characteristic of most solid tumors. TIFP may hamper adequate uptake of macromolecular therapeutics in tumor tissue. In addition, TIFP generates mechanical forces affecting the tumor cortex, which might influence the growth parameters of tumor cells. This seems likely as, in other tissues (namely, blood vessels or the skin), mechanical stretch is known to trigger proliferation. Therefore, we hypothesize that TIFP-induced stretch modulates proliferation-associated parameters. Solid epithelial tumors (A431 and A549) were grown in Naval Medical Research Institute nude mice, generating a TIFP of about 10 mm Hg (A431) or 5 mm Hg (A549). Tumor drainage of the central cystic area led to a rapid decline of TIFP, together with visible relaxation of the tumor cortex. It was found by sodium dodecyl sulfate polyacrylamide gel electrophoresis and Western blot analysis that TIFP lowering yields a decreased phosphorylation of proliferation-associated p44/42 mitogen-activated protein kinase and tumor relaxation. In confirmation, immunohistochemical staining showed a decrease of tumor-associated proliferation marker Ki-67 after TIFP lowering. These data suggest that the mechanical stretch induced by TIFP is a positive modulator of tumor proliferation.
Meeting Abstract Es wurde eine zellbasierte Wundauflage mit Keratinozyten und Fibroblasten auf Basis einer kommerziellen Wundauflage (Matriderm, Collagen/Elastin-Matrix) generiert, um damit großflächige Verbrennungswunden behandeln zu können. Zunächst wurde die Expansion der Keratinozyten optimiert und die Zeit für die Anzüchtung minimiert. Ausgangsmaterial waren 1–2 cm2 Spalthaut vom Patienten. Epidermis und Dermis wurden nach einer enzymatischen Behandlung mit Thermolysin voneinander getrennt. Aus den beiden Hautkompartimenten wurden durch Trypsin- und Kollagenase I-Behandlung Keratinozyten und Fibroblasten isoliert, welche in Kollagen I-beschichteten Zellkulturflaschen expandiert wurden. Nach 10 Tagen wurden die Fibroblasten auf 100 cm2 Matriderm aufgebracht. Nach einwöchiger submerser Kultivierung wurden die Keratinozyten ausgesät. Eine Woche später wurde die Matrix an die Luft-Flüssigkeitsgrenze angehoben, um die epidermale Differenzierung einzuleiten. Nach 16 Tagen wurde das Hautäquivalent fixiert und immunhistologisch sowie elektronen-mikroskopisch begutachtet. Die Histologie zeigte eine regelgerechte Stratifizierung des epidermalen Anteils. Immunhistologisch ließ sich eine Basalmembran mit Collagen IV und Laminin 5 nachweisen. Proliferative Zellen, nachgewiesen mit KI-67 befanden sich lediglich in der basalen Region der Epidermis. Desmoglein, sowie die Differenzierungsmarker Involucrin und CK 10 wurden suprabasal nachgewiesen. Elektronenmikroskopisch waren die Basalmembran sowie die Zell-Zell-Verbindungen in Form von Desmosmen zu erkennen. Späte Differenzierungsmerkmale, wie granuläre Strukturen und verdickte Zellmembranen, fanden sich im Str. granulosum und Str. corneum. Die Studie zeigt, dass man aus Matriderm eine zellbasierte Wundauflage herstellen kann, die verglichen mit dem Ausgangsmaterial um den Faktor 50–100 vergrößert ist und deren Aufbau normaler Haut weitgehend entspricht.
Mantle cell lymphoma (MCL) is a unique type of B-cell non-Hodgkin's lymphoma, which very rarely exhibits skin involvement. We herein describe the case of a 55-year-old woman, who initially presented with a nodular mass of the right infraorbital region. On histological analysis of the subcutaneous tissue, a diffuse neoplastic cell infiltration was identified, composed of medium‑sized lymphoid cells with irregular nuclei, which was diagnosed as MCL. The tumor cells were positive for CD5, CD20, CD79a, cyclin D1 and sex‑determining region Y-box 11, but negative for CD10 and CD23. Our patient received six cycles of R‑CHOP chemotherapy and intrathecal methotrexate as central nervous system prophylaxis. However, the patient relapsed 1 year later and was treated with two cycles of R‑DHAP and one cycle of intrathecal methotrexate. After achieving partial remission, the patient was consolidated with peripheral blood stem cell transplantation using the BEAM conditioning regime. While prior case studies suggest that skin invasion by MCL is associated with a poor prognosis, our patient remains alive almost 4 years after the initial presentation. Skin involvement as a first sign of systemic MCL is very rare and must be considered.