Expression of the Tumor Necrosis Factor Gene by Dermal Fibroblasts in Response to Ultraviolet Irradiation or Lipopolysaccharide

Abstract

To examine the effects of different wavelengths of ultraviolet (UV) radiation on tumor necrosis factor (TNF) production, we took advantage of mice carrying a chloramphenicol acetyl transferase (CAT) reporter transgene bearing the entire TNF promoter and 3'-untranslated region. Aside from constitutive expression in the thymus, CAT activity was detected only in locally UVB- or UVC-irradiated skin. After UVB irradiation, markedly greater amounts of CAT activity were traced to the dermis rather than the epidermis; by contrast, almost all CAT activity was localized to the epidermis after UVC irradiation. Fibroblasts have not been shown previously to express the TNF gene, i.e., the TNF gene is highly methylated and inaccessible to exogenous modulation in 3T3 fibroblasts. However, the present report reveals that cultured dermal fibroblasts are capable of producing both CAT and TNF in response to treatment in vitro with either UVB irradiation, UVC irradiation, or lipopolysaccharide. These findings indicate that dermal fibroblasts may serve not only as a target for but also as a source of TNF.

UVB Radiation-Mediated Expression of Inducible Nitric Oxide Synthase Activity and the Augmenting Role of Co-Induced TNF-α in Human Skin Endothelial Cells

“…As UVB radiation is known to induce TNF-a expression in dermal cells (de Kossodo et al, 1995;Strickland et al, 1997), we next examined whether the UVB-induced effects or parts of it are under the influence of endogenous endothelial TNF-a production.…”

Stress-Induced Fas Ligand Expression in T Cells Is Mediated through a MEK Kinase 1-Regulated Response Element in the Fas Ligand Promoter

“…In this regard, DA-MEKK1 has been demonstrated to induce TNF-␣ secretion in mast cells in parallel with transcriptional activation of the TNF-␣ promoter (24). TNF-␣ secretion may serve as an alternative or complementary mechanism which contributes to stress-induced apoptosis (11). The use of one or both mechanisms may differ from tissue to tissue or stimulus to stimulus.…”

Low-Dose UVB Contributes to Host Resistance againstLeishmania amazonensisInfection in Mice through Induction of Gamma Interferon and Tumor Necrosis Factor Alpha Cytokines

“…Lane SM, size markers. serum TNF-␣ and TNF-␣ mRNA in human and mouse keratinocytes and in dermal fibroblasts were induced by UVB irradiation at doses of 2, 10 to 100, and 1,400 J/m 2 , respectively (9,24,25). Considering these findings, it is highly possible that UVB at a dose of 250 J/m 2 will exert a protective effect on the course of L. amazonensis infection, i.e., delaying and significantly suppressing lesion development in irradiated mice compared to nonirradiated control mice.…”