Low prevalence of oral and nasal human papillomavirus in employees performing CO2-laser evaporation of genital warts or loop electrode excision procedure of cervical dysplasia.

Risk of human papillomavirus (HPV) transmission during laser vaporisation of genital warts or loop electrode excision procedure is controversial. An oral rinse, a nasal swabs, history of HPV related diseases and data on HPV exposure were collected from 287 employees at departments of dermato-venerology and gynaecology in Denmark. A mucosal HPV type was found among 5.8% of employees with experience of laser treatment of genital warts as compared to 1.7% of those with no experience (p = 0.12). HPV prevalence was not higher in employees participating in electrosurgical treatment or cryotherapy of genital warts, or loop electrode excision procedure compared with those who did not. HPV 6 or 11 were not detected in any samples. Hand warts after the age of 24 years was more common among dermatology than among non-dermatology personnel (18% vs. 8.0%, p = 0.03). Mucosal HPV types are infrequent in the oral and nasal cavity of health care personnel, however, employees at departments of dermato-venereology are at risk of acquiring hand warts.

Glucocorticoid-induced tumour necrosis factor receptor (GITR) and its ligand (GITRL) in atopic dermatitis.

The glucocorticoid-induced tumour necrosis factor receptor-related gene (GITR) is expressed on regulatory T-cells (Treg), which are CD4+CD25+ lymphocytes. Binding of the GITR-ligand (GITRL) leads to downregulation of the regulatory function of Tregs. Patients suffering from a defect in their Tregs exhibit a condition in their skin resembling atopic dermatitis. GITR also exists in a soluble form, and increased levels of this lead to decreased levels of GITRL and thereby increased Treg activity. We have measured the levels of GITR and GITRL in plasma from atopic dermatitis patients and found it not to be increased. Furthermore, plasma levels of GITR and GITRL did not correlate with SCORAD. Both GITR and GITRL correlated with the levels of thymus- and activation-regulated chemokine/CCL17 and cutaneous T-cell-attracting chemokine/CCL27, two chemokines believed to play a major role in the pathogenesis of atopic dermatitis and the migration of Tregs and skin-homing T-cells. Immunohistochemistry showed GITR and GITRL were present in few dermal cells of both patients with atopic dermatitis, and normal healthy volunteers, and often localized in close proximity to each other. Since regulatory T-cells are localized in the vicinity of GITRL-expressing cells in atopic dermatitis skin, the GITR/GITRL interaction may serve to perpetuate the inflammation locally.

Expression of CCR2 on monocytes and macrophages in chronically inflamed skin in atopic dermatitis and psoriasis.

Monocytes form a significant component of the inflammatory reaction taking place in the skin of atopic dermatitis and psoriasis. Chemokines are pivotal in mediating the attraction of leucocytes to sites of inflammation. The CC-chemokine, monocyte chemotactic protein 1 (MCP-1/CCL2), is expressed by keratinocytes in both atopic dermatitis and psoriasis. MCP-1 binds to the chemokine receptor CCR2 which is known to be expressed on monocytes and macrophages. We examined the expression of CCR2 on peripheral blood monocytes from patients with psoriasis (n=8) and atopic dermatitis (n=7) and found it to be expressed on approximately 90% of the cells, whereas monocytes from healthy donors had a significantly lower CCR2 expression (p<0.05). Skin biopsies from patients suffering from atopic dermatitis and psoriasis revealed that CCR2-positive cells expressed CD163, a marker for monocytes/macrophages. However, not all CD163-positive cells expressed CCR2, which could be interpreted as a mechanism for retaining the macrophages in the skin. Furthermore, we found that keratinocytes are able to express MCP-1, when stimulated with tumour necrosis factor-alpha and/or interferon-gamma in a dose-dependent manner. Thus MCP-1 and CCR2 interaction is likely of importance for the monocyte/macrophage trafficking of inflammatory skin disorders.