scholarly journals Update of Immune Events in the Murine Contact Hypersensitivity Model: Toward the Understanding of Allergic Contact Dermatitis

2013 ◽  
Vol 133 (2) ◽  
pp. 303-315 ◽  
Author(s):  
Tetsuya Honda ◽  
Gyohei Egawa ◽  
Stephan Grabbe ◽  
Kenji Kabashima
Keyword(s):  
Contact Dermatitis ◽  
Allergic Contact Dermatitis ◽  
Contact Hypersensitivity ◽  
Allergic Contact

scholarly journals Cl− channel is required for CXCL10-induced neuronal activation and itch response in a murine model of allergic contact dermatitis

2017 ◽  
Vol 118 (1) ◽  
pp. 619-624 ◽  
Author(s):  
Lintao Qu ◽  
Kai Fu ◽  
Steven G. Shimada ◽  
Robert H. LaMotte
Keyword(s):  
Contact Dermatitis ◽  
Allergic Contact Dermatitis ◽  
Murine Model ◽  
Behavioral Effects ◽  
Contact Hypersensitivity ◽  
Squaric Acid ◽  
Neuronal Activation ◽  
Ionic Mechanisms ◽  
Cxcr3 Signaling ◽  
Allergic Contact

Persistent itch often accompanies allergic contact dermatitis (ACD), but the underlying mechanisms remain largely unexplored. We previously demonstrated that CXCL10/CXCR3 signaling activated a subpopulation of cutaneous primary sensory neurons and mediated itch response after contact hypersensitivity (CHS), a murine model of ACD, induced by squaric acid dibutylester. The purpose of this study was to determine the ionic mechanisms underlying CXCL10-induced neuronal activation and allergic itch. In whole cell recordings, CXCL10 triggered a current in dorsal root ganglion (DRG) neurons innervating the area of CHS. This current was modulated by intracellular Cl− and blocked by the general Cl− channel inhibitors. Moreover, increasing Ca2+ buffering capacity reduced this current. In addition, blockade of Cl− channels significantly suppressed CXCL10-induced Ca2+ response. In behavioral tests, injection of CXCL10 into CHS site exacerbated itch-related scratching behaviors. Moreover, the potentiating behavioral effects of CXCL10 were attenuated by either of two Cl− channel blockers. Thus we suggest that the Cl− channel acts as a downstream target mediating the excitatory and pruritic behavioral effects of CXCL10. Cl− channels may provide a promising therapeutic target for the treatment of allergic itch in which CXCL10/CXCR3 signaling may participate. NEW & NOTEWORTHY The ionic mechanisms underlying CXCL10-induced neuronal activation and allergic itch are largely unexplored. This study revealed that CXCL10 evoked an ionic current mainly carried by Cl− channels. We suggest that Cl− channels are likely key molecular candidates responsible for the CXCL10-evoked neuronal activation and itch-like behaviors in a murine model of allergic contact dermatitis induced by the antigen squaric acid dibutylester. Cl− channels may emerge as a promising drug target for the treatment of allergic itch in which CXCL10/CXCR3 signaling may participate.

scholarly journals Contact hypersensitivity and allergic contact dermatitis among school children and teenagers with eczema

2009 ◽  
Vol 60 (5) ◽  
pp. 264-269 ◽  
Author(s):  
Ewa Czarnobilska ◽  
Krystyna Obtulowicz ◽  
Wojciech Dyga ◽  
Katarzyna Wsolek-Wnek ◽  
Radoslaw Spiewak
Keyword(s):  
Contact Dermatitis ◽  
Allergic Contact Dermatitis ◽  
School Children ◽  
Contact Hypersensitivity ◽  
Allergic Contact

scholarly journals Immunosuppressive effect of hispidulin in allergic contact dermatitis

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Premrutai Thitilertdecha ◽  
Panwadee Pluangnooch ◽  
Sunita Timalsena ◽  
Kitipong Soontrapa
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Contact Dermatitis ◽  
Allergic Contact Dermatitis ◽  
Contact Hypersensitivity ◽  
Immunosuppressive Effect ◽  
Flavonoid Compound ◽  
Dependent Manner ◽  
Ifn Γ ◽  
Allergic Contact

Abstract Background Long-term use of most immunosuppressants to treat allergic contact dermatitis (ACD) generates unavoidable severe side effects, warranting discovery or development of new immunosuppressants with good efficacy and low toxicity is urgently needed to treat this condition. Hispidulin, a flavonoid compound that can be delivered topically due to its favorable skin penetrability properties, has recently been reported to possess anti-inflammatory and immunosuppressive properties. However, no studies have investigated the effect of hispidulin on Th1 cell activities in an ACD setting. Methods A contact hypersensitivity (CHS) mouse model was designed to simulate human ACD. The immunosuppressive effect of hispidulin was investigated via ear thickness, histologic changes (i.e., edema and spongiosis), and interferon-gamma (IFN-γ) gene expression in 1-fluoro-2,4-dinitrobenzene (DNFB)-sensitized mice. Cytotoxicity, total number of CD4+ T cells, and percentage of IFN-γ-producing CD4+ T cells were also investigated in vitro using isolated CD4+ T cells from murine spleens. Results Topically applied hispidulin effectively inhibited ear swelling (as measured by reduction in ear thickness), and reduced spongiosis, IFN-γ gene expression, and the number of infiltrated immune cells. The inhibitory effect of hispidulin was observed within 6 h after the challenge, and the observed effects were similar to those effectuated after dexamethasone administration. Hispidulin at a concentration up to 50 μM also suppressed IFN-γ-producing CD4+ T cells in a dose-dependent manner without inducing cell death, and without a change in total frequencies of CD4+ T cells among different concentration groups. Conclusion The results of this study, therefore, suggest hispidulin as a novel compound for the treatment of ACD via the suppression of IFN-γ production in Th1 cells.

Contribution of CD4+and CD8+T-cells in contact hypersensitivity and allergic contact dermatitis

2005 ◽  
Vol 1 (1) ◽  
pp. 75-86 ◽  
Author(s):  
Marc Vocanson ◽  
Ana Hennino ◽  
Cyril Chavagnac ◽  
Pierre Saint-Mezard ◽  
Bertrand Dubois ◽  
...  
Keyword(s):  
T Cells ◽  
Contact Dermatitis ◽  
Allergic Contact Dermatitis ◽  
Cd8 T Cells ◽  
Contact Hypersensitivity ◽  
Allergic Contact
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