Ratite oils promote keratinocyte cell growth and inhibit leukocyte activation.

Traditionally, native Australian aborigines have used emu oil for the treatment of inflammation and to accelerate wound healing. Studies on mice suggest that topically applied emu oil may have anti-inflammatory properties and may promote wound healing. We investigated the effects of ratite oils (6 emu, 3 ostrich, 1 rhea) on immortalized human keratinocytes (HaCaT cells) in vitro by culturing the cells in media with oil concentrations of 0%, 0.5%, and 1.0%. Peking duck, tea tree, and olive oils were used as comparative controls. The same oils at 0.5% concentration were evaluated for their influence on peripheral blood mononuclear cell (PBMC) survival over 48 hr and their ability to inhibit IFNγ production in PBMCs activated by phytohemagglutinin (PHA) in ELISpot assays. Compared to no oil control, significantly shorter population doubling time durations were observed for HaCaT cells cultured in emu oil (1.51×faster), ostrich oil (1.46×faster), and rhea oil (1.64×faster). Tea tree oil demonstrated significant antiproliferative activity and olive oil significantly prolonged (1.35×slower) cell population doubling time. In contrast, almost all oils, particularly tea tree oil, significantly reduced PBMC viability. Different oils had different levels of inhibitory effect on IFNγ production with individual emu, ostrich, rhea, and duck oil samples conferring full inhibition. This preliminary investigation suggests that emu oil might promote wound healing by accelerating the growth rate of keratinocytes. Combined with anti-inflammatory properties, ratite oil may serve as a useful component in bandages and ointments for the treatment of wounds and inflammatory skin conditions.

Somatostatin expression in human hair follicles and its potential role in immune privilege.

Immune privilege (IP) is believed to exist in the anagen hair follicle (HF). Studies have shown that downregulation of major histocompatibility complex Class I occurs and immunosuppressive factors are expressed in the HF bulb and bulge. However, demonstration and quantification of functional IP in HF cells are required. We examined the middle (sheath) and lower (bulb) portions of the human HF using quantitative real-time RT-PCR (qPCR), immunohistology, ELISA, in vitro coculture with peripheral blood mononuclear cells (PBMCs), and flow cytometry. We found that HF cells, relative to non-follicular epidermal cells, failed to promote allogeneic PBMC proliferation and CD4(+) and CD8(+) IFNγ production. By qPCR, we found significant downregulation of Class I and Class II HLA alleles in both the bulb and sheath, and upregulation of multiple immunoregulatory genes. It is noteworthy that somatostatin (SST) was significantly upregulated relative to epidermis. By immunohistochemistry, SST was most strongly expressed in the HF outer root sheath, and, by ELISA, cultured sheath cells secreted SST. PBMCs, cultured with stimulatory allogeneic epidermal cells and SST, secreted significantly less IFNγ than controls. Addition of SST antagonists to PBMCs cocultured with allogeneic HF cells increased IFNγ secretion. The data identify SST as a secretory factor potentially contributing to the HF IP repertoire.

Lichen planopilaris and pseudopelade of Brocq involve distinct disease associated gene expression patterns by microarray.

BACKGROUND: Lichen planopilaris (LPP) and pseudopelade of Brocq (PPB) are two scarring alopecia diagnoses that exhibit similar clinical features. Some suggest LPP and PPB are not distinct diseases, but rather different clinical presentations in a spectrum derived from the same underlying pathogenic mechanism. OBJECTIVE: We explored the degree of similarity between LPP and PPB gene expression patterns and the potential for common and unique gene pathway and gene activity in LPP and PPB using microarrays. METHODS: Microarray analysis, using a 21K cDNA set, was performed on pairs of biopsies obtained from affected and unaffected scalp of untreated patients. Diagnosis was confirmed by histopathology. Significantly differentially expressed genes were identified by analysis of microarray results in various datasets and screened for signaling pathway involvement. Selected genes were validated by quantitative PCR and immunohistology. RESULTS: The global gene expression profiles in LPP and PPB versus comparative intra-control scalp tissue were distinguishable by significance analysis of microarrays (SAM). There was limited commonality in the gene expression profiles between LPP and PPB. Specific genes, such as MMP11, TNFSF13B, and APOL2, were identified with significantly differential expression in association with LPP versus PPB. CONCLUSIONS: Our findings may have important implications for understanding the pathogenesis of LPP and PPB at the molecular level. Results suggest LPP and PPB involve different mechanisms of disease development and should be regarded as biologically distinct cicatricial alopecia diagnoses. Genes that we have identified may be useful as markers of the respective diagnoses and may be potential therapeutic targets.