Human beta defensin-1 and -2 expression in human pilosebaceous units: upregulation in acne vulgaris lesions.

A rich residential microflora is harboured by the distal outer root sheath of the hair follicle and the hair canal - normally without causing skin diseases. Although the basic mechanisms involved in the development of inflammation during acne vulgaris remain unclear, microbial agents might play an important role in this process. In this study we have analyzed by in situ hybridization and immunohistochemistry the expression patterns of two antimicrobial peptides, human beta defensin-1 and human beta defensin-2, in healthy human hair follicles as well as in perilesional and intralesional skin of acne vulgaris lesions such as comedones, papules, and pustules. Strong defensin-1 and defensin-2 immunoreactivity was found in all suprabasal layers of the epidermis, the distal outer root sheath of the hair follicle, and the pilosebaceous duct. Marked defensin-1 and defensin-2 immunoreactivity was also found in the sebaceous gland and in the basal layer of the central outer root sheath including the bulge region. The majority of acne biopsies displayed a marked upregulation of defensin-2 immunoreactivity in the lesional and perilesional epithelium - in particular in pustules - and a less marked upregulation of defensin-1 immunoreactivity. The upregulation of beta-defensin expression in acne vulgaris lesions compared to controls suggests that beta-defensins may be involved in the pathogenesis of acne vulgaris.

Laser modulation of angiogenic factor production by T-lymphocytes.

BACKGROUND AND OBJECTIVE: In previous investigations, small variations in the energy densities of low level light therapy (LLLT) were found to produce significant differences in the proliferation of resting T-lymphocytes in vitro. Pulsing these cells with mitogen in addition to laser therapy produced inhibitory effects regardless of the amplitude of the energy density used. In the current study, the effect of LLLT on the production of angiogenic factor(s) by T-lymphocytes was investigated in vitro. STUDY DESIGN/MATERIALS AND METHODS: Human T-cells isolated from peripheral blood were prepared in suspension either with or without addition of mitogen. Cell suspensions were irradiated with laser by using the following energy densities: 1.2, 3.6, 6.0, and 8.4 J/cm(2). Wavelength, pulsing frequency, and power output were kept constant at 820 nm, 5,000 Hz, and 50 mW, respectively. After either 3 or 5 days of incubation, lymphocyte supernatants were collected and added as conditioned media to cultured endothelial cells (ECs). The effect on the proliferation of these ECs was assessed over a 72-hour period by using a methylene blue assay. RESULTS: Endothelial cell proliferation increased significantly when incubated with conditioned media collected from resting T-cells exposed to 1.2 and 3.6 J/cm(2). Day 5 conditioned media produced similar patterns of EC proliferation to that of day 3 but at lower magnitude. Pulsing of T-lymphocytes with mitogen in addition to laser irradiation significantly lessened their angiogenic capability. Conditioned media from 3.6 J/cm(2) laser-treated T-cells induced the maximal EC proliferation in all groups studied. CONCLUSION: It would seem that laser therapy stimulates lymphocytes to produce factor(s) that can modulate EC proliferation in vitro; this effect on the lymphocytes is influenced by (1) the amplitude of energy density used for T-cell irradiation, (2) exposing T-cells to both mitogen and laser, and (3) the duration of T-cell incubation in culture.