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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 548 (1988), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Clinical and experimental dermatology 26 (2001), S. 0 
    ISSN: 1365-2230
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Leukaemia inhibitory factor (LIF) and interleukin (IL)-8 possess activities which may contribute to the development of carcinomas. LIF can stimulate proliferation of some tumour cell lines and IL-8 is angiogenic. Using semiquantitative reverse-transcription polymerase chain reaction (RT–PCR), we measured the expression of LIF and IL-8 mRNA in cultured normal keratinocytes (NKC) and the malignant carcinoma cells lines A431, SiHa, HeLa, and in biopsies of basal cell carcinoma (BCC), squamous cell carcinoma (SCC) and normal skin. Protein expression for LIF was assessed by immunohistochemistry in the biopsies. LIF mRNA expression was increased significantly (P 〈 0.01) in all carcinoma lines, except SiHa, compared with NKC but the IL-8 mRNA expression in carcinoma cell lines was similar to that in NKC. Expression of LIF mRNA was elevated in BCC and SCC compared with normal skin, but a significant difference was observed only between SCC and normal skin (P 〈 0.01). Both BCC and SCC showed significantly greater expression of IL-8 compared with normal skin (P 〈 0.01). There was no correlation between LIF and IL-8 mRNA expression either in BCCs or in SCCs. Immunoreactivity for LIF was absent throughout BCC and SCC, however, normal epidermis surrounding the tumour stained positive, as in normal skin. These data may suggest a role for LIF and IL-8 in the development of skin carcinomas, but without co-ordinate regulation of these two cytokines in this process.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract Conflicting reports exist concerning ultraviolet-B (UVB) effects on keralinocyte (KC) interleukin-l (IL-1) expression. To clarify the modulatery effects of UVB on IL-1, the following study was undertaken. Normal human epidermal KCs cultured in a standard low Ca2+ and serum-free medium were irradiated in quiescent phase with UVB. In this study, we used semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) to determine the mRNA level of interleukin-1α (IL-1α) and interleukin-1β (IL-β). After exposure to 100 or 300 J/m2 UVB, a transient increase in mRNA levels was observed within I hour for IL-1α and 3 to 6 h for IL-β Following this transient induction, mRNA levels for both IL-1α and IL-1β returned to steady-state levels after 100 J/m2. After 300 J/m2 irradiation, IL-1α and IL-1β levels were downregulated compared to unirradiated cultures at 24-h post-irradiation. The half-life for IL-1α and IL-1β was estimated using actinomycin D treatment. Both IL-1α and IL-1β mRNAs half-lives (t1/2) decreased faster in irradiated cells (t1/2 = 30 minutes for IL-1α and 2 h for IL-1β) compared to unirradiated cells (t1/2= 1 h and 4 h, respectively). These results suggest that IL-1α and IL-1β mRNA expression are differentially regulated by UVB. In contrast to down-regulation of mRNA levels, a significant increase in IL-1α protein levels, measured by ELISA. was observed in culture supernatant from 6 h to 24 h after 300 J/m2 UVB irradiation. Cycloheximide treatment did not abrogate this increase in IL-1α protein level. Since this dose of UVB irradiation decreased the stability of IL-1α and IL-1β mRNA, this suggests that the release of IL-1α after UVB irradiation was due to leakage from UVB-damaged cells and not from de novo protein synthesis.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract Ultraviolet radiation can induce the transcription and release of cytokines From keratinocytes (KC's). These cytokines have the potential to modulate local and systemic immunologic responses. In this paper we report that northern blotting showed that human KC and KC lines expressed a 1.2-1.4 kb transcript for the chemokine and melanoma growth-stimulatory protein, GRO-α and that ultraviolet B radiation (UVB) could upregulate the expression of GRO-α mRNA and protein in the KC line A431. The GRO-α gene response to UVB was maximal at 48h post-irradiation with 70 J/m2. Reverse transcription-polymerase chain reaction (RT-PCR) revealed a 4.5-fold increase in GRO-α mRNA over basal levels (p〈0.001). GRO-α protein was measured in the culture media by enzyme-linked immunosorbent assay (ELISA). Media from unirradiated cultures contained 1166±83 pg/ml GRO-α protein. After UVB, a time-dependent increase in GRO-α protein was seen in the culture media from 6-48h. At 48h post-irradiation the GRO-α protein content was 27583±678 pg/ml, or 23 times the basal level. This protein release could be inhibited by 70% when the cells were pre-incubated with 10 μg/ml interleukin-1 receptor antagonist (IL-1RA). We also show that another potent leukocyte chemoattractant, Interleukin-8 (IL-8), was induced in A431 cells by UVB. The induction of IL-8 mRNA began as early as 3h post-irradiation, when it reached twice basal levels (p〈0.05) and reached 4.5-fold basal levels at 48h post-irradiation (p〈0.005). Analysis of the conditioned media from the irradiated cells by ELISA revealed that IL-8 protein accumulation was increased from 162± 16 pg/ml (unirradiated cultures) to 993± 120 pg/ml 24h post-irradiation. The accumulation increased to 1383± 178 pg/ml, or 9-fold the basal level by 48h post-irradiation. Thus keratinocytes are capable of generating chemoattractant factors which enhance melanoma growth after UVB irradiation, which may contribute to the inflammatory infiltrate found in the dermis of sunburned skin.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 289 (1996), S. 28-34 
    ISSN: 1432-069X
    Keywords: Key words Human papillomavirus ; Cytokine ; Amphiregulin ; Cutaneous warts ; Interleukin-1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The persistence of human papillomavirus at cutaneous sites may be due to impaired trafficking of immune effector cells to the epidermis. We investigated whether HPV infection modulates cytokine mRNA expression in skin, thereby influencing local immunity. The mRNA expression of tumour necrosis factor-α, interleukin-1α (IL-1α), IL-1β, IL-1 receptor antagonist (IL-1ra), IL-4, IL-8, IL-10, IL-12, granulocyte macrophage colony-stimulating factor, transforming growth factor-β, interferon-γ and amphiregulin were assayed in cutaneous warts and normal skin by semiquantitative reverse transcriptase-polymerase chain reaction. The expression of the cytokines was heterogeneous in the specimens but, of the 12 mRNA species investigated, only IL-10 mRNA was significantly downregulated in warts compared with normal skin ( P = 0.002). IL-1α mRNA expression was significantly upregulated in common warts ( P = 0.019) and plantar warts ( P = 0.003) compared with normal skin. The expression of IL-1α and IL-1ra mRNAs were significantly correlated in plantar warts ( P 〈 0.05). Warts expressing IL-1α also expressed amphiregulin, and there was a significant correlation between the expression of these two genes ( P 〈 0.05). It is possible that IL-1α expression in cutaneous warts may modulate the growth of papillomavirus-infected keratinocytes, mediated by amphiregulin, thus ensuring viral persistence.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-069X
    Keywords: Key words eNOS ; Melanocytes ; Keratinocytes ; Nitric oxide ; RT-PCR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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