These data document for the first time itch-related local markers in psoriasis, and suggest complex and multifactorial mechanisms of pruritus in the disease. These results provide the groundwork for further studies to evaluate the efficacy of antipruritic treatment for psoriatic patients.

These data represent the first reported evidence of increased plasma levels of NGF and SP in an allergic human skin disease. They suggest that these neurogenic factors systemically modulate the allergic response in AD, probably through interactions with cells of the immune-inflammatory component. In addition, NGF and SP may be useful markers of disease activity in patients with AD.

Acne vulgaris is a skin disorder of the sebaceous follicles that commonly occurs in adolescence and in young adulthood. The major pathogenic factors involved are hyperkeratinization, obstruction of sebaceous follicles resulting from abnormal keratinization of the infundibular epithelium, stimulation of sebaceous gland secretion by androgens, and microbial colonization of pilosebaceous units by Propionibacterium acnes, which promotes perifollicular inflammation. The clinical presentation of acne can range from a mild comedonal form to severe inflammatory cystic acne of the face, chest, and back. At the ultrastructural level, follicular keratinocytes in comedones can be seen to possess increased numbers of desmosomes and tonofilaments, which result in ductal hypercornification. The increased activity of sebaceous glands elicited by androgen causes proliferation of P. acnes, an anaerobe present within the retained sebum in the pilosebaceous ducts. The organism possesses a ribosome-rich cytoplasm and a relatively thick cell wall, and produces several biologically active mediators that may contribute to inflammation, for instance, by promoting leukocyte migration and follicular rupture. In inflamed lesions, numerous neutrophils and macrophages infiltrate around hair follicles and sometimes phagocytose P. acnes. To examine the participation of neurogenic factors in the pathogenesis of acne, we quantitatively assessed the effects of neuropeptides on the morphology of sebaceous glands in vitro using electron microscopy. Substance P, which can be elicited by stress, promoted the development of cytoplasmic organelles in sebaceous cells, stimulated sebaceous germinative cells, and induced significant increases in the area of sebaceous glands. It also increased the size of individual sebaceous cells and the number of sebum vacuoles for each differentiated sebaceous cell, all of which suggests that substance P promotes both the proliferation and the differentiation of sebaceous glands. In this review, we introduce the general concept of pathogenic factors involved in acne, including typical electron microscopic findings and recent evidence of stress-induced exacerbation of acne from a neurological point of view. An improved understanding of the pathogenesis of acne should lead to a rational therapy to successfully treat this skin disease.

The skin of AD patients was more frequently colonized with S. aureus than that of normal controls. As the severity of the AD lesions increased, the numbers of S. aureus isolated increased. The skin of HS was more colonized with S. epidermidis. Other species of CNS were isolated from several cases of AD patients and HS. In addition, S. aureus, S. epidermidis, and the other CNS showed poor susceptibility to some of the tested antimicrobial drugs.

We previously isolated a new member of the fusedtype S100 protein family (hornerin) from the mouse (Makino, T., Takaishi In this study, we identified and partially characterized a human ortholog of mouse hornerin. The human hornerin gene was mapped between trichohyalin and filaggrin on chromosome 1q21.3, the region being completely syntenic with the counterpart of the mouse. The deduced amino acid sequence of 2850 residues shows typical structural features of "fused-type" S100 protein family members. Mature transcripts and protein from human hornerin were not detected in normal stratified epithelium, including the trunk epidermis, tongue, and esophagus. After screening of various normal and pathological human tissues, we found that human hornerin was expressed in psoriatic skin. Hornerin protein was present in the keratinizing region, although at a lower level and in fewer cells compared with filaggrin. Mature transcripts and protein from hornerin were also detected in regenerating human skin after wounding. Hornerin mRNA was induced 5 days after wounding. The mRNA level remained almost constant until 15 days and declined at 30 days after wounding. Hornerin protein was detected in the proximal epidermis (but not in the distal epidermis) at 15 days after wounding. These results indicate that hornerin has a function similar to but distinct from that of filaggrin in cornification.