Journal of dermatological science
-
Repeated ultraviolet (UV) irradiations have been shown to induce keratinocyte proliferation with acanthosis, stimulate the cutaneous nerve proliferation, and increase the synthesis of calcitonin gene-related peptide (CGRP). In the current study, we examined the role of CGRP in the UVB-induced proliferation of murine keratinocytes. UVB irradiation increased the number of bromodeoxyuridine (BrdU)-labeled basal keratinocytes and caused acanthosis. ⋯ Intradermal injections of anti-CGRP antibody inhibited the UVB-induced BrdU labeling in basal keratinocytes, but epidermal thickening was not significantly inhibited. These results indicate that CGRP is one of the stimulators to UVB-induced keratinocyte proliferation. On the other hand, expression of substance P, another neuropeptide in the peripheral nerve, was not up-regulated by UVB irradiation.
-
Defensins, a major family of antimicrobial peptides, are small cationic, cysteine-rich peptides with a wide range of antimicrobial activity. In human, beta-defensin-1 was isolated from urine and cervical mucous suggesting that this peptide plays an antimicrobial role in the genitourinary tract. Beta-defensin-2 was identified in psoriatic scale produced by keratinocytes suggesting that this peptide contributes to defend the expansive surface of the integuments. ⋯ This report demonstrates the presence of defensin in human keratinocytes and capacity of human keratinocytes to produce defensin mRNA in response to UVB irradiation, TNF-alpha and LPS. Release of defensins by keratinocytes in response to cytokines elaborated in inflammation may contribute to the host defense responses.
-
To clarify the behavioral and pathological features of spontaneous scratching of NC mice with mite-induced chronic dermatitis, we investigated the spontaneous and pruritogen-evoked scratching of NC mice. Although the frequency of scratching of NC mouse did not increase under specific pathogen-free environment, it gradually and markedly increased from 3 to 6 weeks after transfer to conventional environment. The onset of increase in spontaneous scratching was similar to that of dermatitis development and the elevation of plasma concentration of immunoglobulin E. ⋯ Methysergide and cyproheptadine inhibited the serotonin-induced scratching but not spontaneous scratching. The results suggest that marked elevation of plasma immunoglobulin E is not always the cause of spontaneous itch-associated response of NC mice with dermatitis. Serotonin, histamine and substance P may not play an important role in spontaneous itch-scratch response at a chronic stage.
-
The human disease xeroderma pigmentosum (XP) involves DNA repair and replication deficiencies that predispose homozygous individuals to a 1000-fold increase in nonmelanoma and melanoma skin cancers. Two major forms of XP are known with different biochemical defects: one form lacks nucleotide excision repair (NER); the other lacks the capacity to replicate damaged DNA. Since the clinical symptoms of both kinds of patients are almost the same, the different cellular defects must be reconciled with common clinical outcomes. ⋯ The presence of unrepaired damage in the NER defective groups of XP would present more substrate for the error-prone system leading to increased mutation rates. The absence of pol eta would require cells to use the error-prone pol zeta pathway, also increasing mutation rates from UV damage. A common pathway for increased mutagenesis therefore underlies both forms of XP.
-
Autoantibodies to human carbonic anhydrase II (CAII) were screened by ELISA in 109 sera from Asian Japanese patients with systemic lupus erythematosus (SLE), primary Sjögren's syndrome (Sjs), progressive systemic sclerosis (PSS) and dermatomyositis (DM). Anti-CAII antibodies were positive in 24.1% of SLE, 20.0% of primary Sjs, 16.7% of PSS and 25.0% of DM. On the other hand, sera from atopic dermatitis, bullous pemphigoid and psoriasis patients showed no activity for anti-CAII antibodies. CAII could be a common exonuclear autoantigen in subsets of rheumatic autoimmune diseases.