The chemokine receptor CCR3 participates in tissue remodeling during atopic skin inflammation.

Background: Recent studies provided insights into the recruitment and activation pathways of leukocytes in atopic dermatitis, however, the underlying mechanisms of tissue remodeling in atopic skin inflammation remain elusive.

Objective: To identify chemokine-mediated communication pathways regulating tissue remodeling during atopic skin inflammation.

Methods: Analysis of the chemokine receptor repertoire of human dermal fibroblasts using flow cytometry and immunofluorescence.

Long-term exposure and health-related quality of life among patients with occupational rhinitis.

Objective: This article evaluates health-related quality of life (HRQoL) among patients with occupational rhinitis (OR), with an average of 10 years after diagnosis.

Methods: A cross-sectional questionnaire with general (RAND-36) and disease-specific (Rhinasthma) HRQoL questions was completed by 119 OR patients and 173 controls of the same age and locality. In addition, the patients compared their estimation of current occupational exposure level with that at the time of OR diagnosis.

Immunostimulatory sequence CpG elicits Th1-type immune responses in inflammatory skin lesions in an atopic dermatitis murine model.

Background: Atopic dermatitis (AD) is a chronic inflammatory skin disease, for which no fundamental therapy exists. Immunostimulatory sequence CpG (ISS CpG) has potential in reducing susceptibility to allergic diseases and reversing established allergic reactions.

Objective: To investigate the effects of ISS CpG in the prevention and treatment of AD in an AD murine model.

Inhalation challenge test in the diagnosis of occupational rhinitis.

Background: Evaluations of rhinitis reactions in inhalation challenges (ICs) are sparse compared with research on nasal challenges. This study evaluates the outcome of IC tests in assessing occupational rhinitis (OR). It presents the largest rhinologic IC data in the literature, analyzing the exposure method of various agents causing OR and their relation to asthma.

Smad3 -signalling and Th2 cytokines in normal mouse airways and in a mouse model of asthma.

This study investigates the role of Smad3 signalling for the T-helper2 (Th2) cytokine homeostasis in normal lungs and in a mouse model of asthma. We used mice deficient for Smad3, a central part of the major signal transduction pathway for TGF-beta and other related cytokines, and a mouse model for allergic asthma with ovalbumin (OVA) as the antigen. Compared to wild type mice, naive (unmanipulated) Smad3-/- mice exhibited significantly increased levels of proinflammatory cytokines and IL-4 as well as the Th2 associated transcription factor GATA-3 in the lung tissue and bronchoalveolar lavage (BAL).

Smad3 signal transducer regulates skin inflammation and specific IgE response in murine model of atopic dermatitis.

Atopic dermatitis (AD) is a common chronic inflammatory skin disease characterized by itchy, dry, and inflamed skin. Transforming growth factor (TGF)-beta is an important fibrogenic and immunomodulatory factor that regulates cellular processes in the injured and inflamed skin. This study examines the role of the TGF-beta-Smad signaling pathway using Smad3-deficient mice in a murine model of AD.

Chemokine responses distinguish chemical-induced allergic from irritant skin inflammation: memory T cells make the difference.

Background: As clinical and histological features of allergic and irritant contact dermatitis share common characteristics, the differentiation between them in the preclinical and clinical evaluations of chemicals remains difficult.

Objective: To identify the differences in the underlying immunological mechanisms of chemical-induced allergic or irritant skin responses.

Methods: We systematically studied the involvement of chemokines in both diseases by quantitative real-time polymerase chain reaction in mice and humans.

IL-31: a new link between T cells and pruritus in atopic skin inflammation.

Background: IL-31 is a novel T-cell-derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of IL-31 receptor A and oncostatin M receptor.

Objective: To investigate the role of human IL-31 in pruritic and nonpruritic inflammatory skin diseases.

Methods: The expression of IL-31 was analyzed by quantitative real-time PCR in skin samples of healthy individuals and patients with chronic inflammatory skin diseases.

Single doses of local betamethasone do not suppress allergic patch test reactions to nickel sulfate.

Topical corticosteroids are usually banned on test areas prior to patch testing. The previous literature on the effect of topical corticosteroids is conflicting. Patients allergic to nickel sulfate were patch tested on 4 sites with nickel on day (D) 0.

CCL27-CCR10 interactions regulate T cell-mediated skin inflammation.

The skin-associated chemokine CCL27 (also called CTACK, ALP and ESkine) and its receptor CCR10 (GPR-2) mediate chemotactic responses of skin-homing T cells in vitro. Here we report that most skin-infiltrating lymphocytes in patients suffering from psoriasis, atopic or allergic-contact dermatitis express CCR10. Epidermal basal keratinocytes produced CCL27 protein that bound to extracellular matrix, mediated adhesion and was displayed on the surface of dermal endothelial cells.