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Biomedical subjects

Mary Norval

Publications and source records attributed to Mary Norval.

23 records · Page 2Linked to original sources

The effects of UV waveband and cis-urocanic acid on tumour outgrowth in mice.

Immunogenic murine tumours that are normally rejected upon transplantation into syngeneic hosts grow progressively if the hosts are UV-irradiated prior to tumour implantation. Using three sources of UV we investigated the most effective waveband and dose for increased outgrowth of injected fibrosarcoma (FSA) cells in mice, compared with unirradiated controls. The animals were exposed on their shaved dorsal skin twice a week for 3 weeks to either broad-band (TL12) or narrow-band (TL01) UVB, or UVA-I radiation; FSA cells were then injected subcutaneously into the UV-irradiated skin. Exposure to TL12 at doses higher than 1000 J m(-2), but not TL01 or UVA-I, caused increased outgrowth of the injected tumour cells. The effect of the UV irradiation seemed to be local as injection of the FSA cells into the unirradiated ventral skin of mice irradiated with TL12 on the dorsal surface did not result in increased outgrowth of the tumours. Cis-urocanic acid, a recognised initiator of UV-induced immunosuppression, applied topically or intradermally for 3 weeks prior to FSA cell injection, had no effect on the rate of tumour outgrowth. Similarly, injection of a monoclonal antibody with specificity for cis-urocanic acid, prior to each irradiation with TL12, did not reverse the increased growth of FSA cells injected into the UV-irradiated skin. Thus wavelengths within the broad-band UVB range are the most effective for inducing increased outgrowth of FSA cells; cis-urocanic acid is not an important mediator in this UV-enhanced growth of tumours.

Animals↗

Systemic immune responses following infection with Jaagsiekte sheep retrovirus and in the terminal stages of ovine pulmonary adenocarcinoma.

Jaagsiekte sheep retrovirus (JSRV) is the aetiological agent of ovine pulmonary adenocarcinoma (OPA). To monitor changes in cellular immune function during JSRV infection, lymphoproliferation in response to various mitogens was measured in the blood of conventionally housed and specific-pathogen-free lambs experimentally infected with JSRV until the development of OPA and compared with uninfected control lambs. In addition, blood samples collected from adult field cases in the terminal stages of OPA and control adult sheep were compared. No difference in the proliferative response to phytohaemagglutinin and pokeweed mitogen between the animal groups was detected. In contrast, reduced responses to concanavalin A stimulation were demonstrated in the JSRV-inoculated lambs, prior to the onset of clinical disease, and also in the terminally ill adult sheep. Peripheral blood leukocytes were monitored to identify phenotypic frequency alterations. The CD4 lymphocytopaenia and neutrophilia reported previously in adult OPA cases were demonstrated but similar phenotypic changes were not identified during experimental infection.

Animals↗

Decrease in langerhans cells and increase in lymph node dendritic cells following chronic exposure of mice to suberythemal doses of solar simulated radiation.

Exposure of certain strains of mice to ultraviolet radiation (UVR) causes suppression of some innate and adaptive immune responses. One such consequence of acute UVB exposure is a reduction in the number of Langerhans cells (LC) in the epidermis and an increase in dendritic cells (DC) in lymph nodes draining the irradiated skin sites. Exposure to chronic UVB irradiation also has effects on the immune system, but it is unknown what effects are caused by repeated doses of solar simulated radiation (SSR). Consequently, the main aims of the present study were to determine whether repeated exposure to low doses of SSR would lead to similar changes in these cell populations and whether chronic doses of SSR activate a protective photoadaptation mechanism. Groups of C3H/HeN mice were irradiated daily with 3.7 J/cm(2) SSR from Cleo Natural lamps for 2, 10, 20, 30 or 60 days. Further groups of mice received an additional dose of 7.4 J/cm(2) SSR on days 2, 10, 30 or 60 to test for photoadaptation. The numbers of LC in the epidermis and DC in the lymph nodes draining irradiated skin sites were counted 24 h after the final irradiation. With the exception of mice irradiated for only 2 days, LC were significantly reduced throughout the chronic irradiation protocol, and no recovery occurred. DC numbers were significantly increased in the draining lymph nodes of mice irradiated for 20 days and 60 days.

Animals↗

The effect of ultraviolet radiation on human viral infections.

Exposure to UV radiation is recognized to suppress cell-mediated immunity and therefore could adversely affect the course of a viral infection. Rodent models of viral infection confirm this possibility but the situation in human subjects is not so clear, apart from two exceptions. These are herpes simplex, in which sunlight exposure can cause reactivation, and certain papillomavirus types in which sunlight exposure can lead to the development of nonmelanoma skin cancer. In both cases, there are UV response elements in the viral genomes that alter the normal interactions between the viruses and the host following exposure, and UV-induced effects on the immune response occur in addition. These complex mechanisms are discussed, and the situation regarding UV radiation and viral exanthems plus other viruses, including the retroviruses, summarized. Finally viral vaccination is considered in the context of UV exposure and the importance of the host's genetic background emphasized. Further research is required to evaluate whether sunlight can significantly affect the resistance to common viral infections and vaccines.

Humans↗