Increased plasma miR-24 and miR-191 levels in patients with severe atopic dermatitis: Possible involvement of platelet activation.

BACKGROUND: Platelets are involved in the pathomechanisms of atopic dermatitis (AD). This study aimed to elucidate the levels of platelet-related miRNAs, (miR-24 and miR-191) in the plasma of AD patients and their relationships with the disease severity and laboratory data. METHODS: miRNAs were detected in the subjects plasma using specifically primed quantitative reverse transcription polymerase chain reaction. RESULTS: The patients with severe AD had significantly higher plasma miR-24 or miR-191 levels than the patients with mild AD, the urticaria patients, and the healthy volunteers. The plasma miR-24 and miR-191 levels of the AD patients were correlated with their serum thymus and activation-regulated chemokine levels. In addition, plasma miR-24 and miR-191 levels were correlated with their plasma levels of platelet factor 4 and ß-thromboglobulin. CONCLUSION: Our findings imply that miR-24 and miR-191 may be involved in the pathomechanisms responsible for the worsening of AD, possibly through their effects on platelet activation.

Effects of constant light exposure on allergic and irritant contact dermatitis in mice reared under constant light conditions.

Environmental light levels can affect physiological functions, such as general activity, body temperature and metabolism. Irregular lifestyles, such as those involving exposure to light during the night, can exacerbate the clinical symptoms of several inflammatory skin diseases. However, the effects of constant light exposure on immune responses are not fully understood. This study aimed to elucidate the effects of constant light exposure on two major types of skin reactions, allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD). BALB/c mice were kept under constant light conditions or a normal light and dark cycle, and their ACD and ICD responses were assessed after the topical application of 2,4,6-trinitro-1-chlorobenzene and croton oil, respectively, to the ear skin. Interestingly, in both ACD and ICD, the ear-swelling response and local leukocyte infiltration were aggravated by constant exposure to light, which has previously been shown to severely disturb the behavioural rhythms of mice. In ACD, these findings were accompanied by increases in the numbers of degranulated mast cells and eosinophils. These results suggest that constant light exposure intensifies allergic and non-allergic skin inflammation.

The role of toll-like receptor 3 in chronic contact hypersensitivity induced by repeated elicitation.

BACKGROUND: Accumulating evidence suggests that Toll-like receptor (TLR)-3 signaling is involved in non-infectious immune and inflammatory reactions as well as in viral infections. The skin of patients with atopic dermatitis (AD) is often infected with virus and bacteria, leading to the aggravation of atopic symptoms. These findings suggest TLR3 signaling may be involved in the pathogenesis of AD, but the exact role of TLR3 in AD remains to be defined. OBJECTIVE: The purpose of this study was to investigate the role of TLR3 in chronic contact hypersensitivity reactions induced by repeated elicitation, resembling the features of AD. METHODS: Wild-type (WT) and Toll-like receptor 3 knockout (Tlr3 KO) mice were sensitized, and chronic contact hypersensitivity reactions were elicited in their ear skin via repeated application of a hapten, 2,4,6-trinitro-1-chlorobenzene (TNCB) or oxazolone. RESULTS: The Tlr3 KO mice exhibited less ear swelling, less leukocyte infiltration into the skin, and lower serum total IgE levels than WT mice after hapten challenge. The Tlr3 KO mice also displayed lower expression levels of inflammatory cytokines (interleukin (IL)-33, IL-4, IL-10, and interferon-ɤ in their TNCB-treated ear skin than WT mice. CONCLUSION: These results showed that TLR3 deficiency suppressed the development of chronic contact hypersensitivity reactions, suggesting that TLR3 signaling may participate in the pathogenesis of AD.