scholarly journals NOD2 and TLR2 ligands trigger the activation of basophils and eosinophils by interacting with dermal fibroblasts in atopic dermatitis-like skin inflammation

2015 ◽  
Vol 13 (4) ◽  
pp. 535-550 ◽  
Author(s):  
Delong Jiao ◽  
Chun-Kwok Wong ◽  
Huai-Na Qiu ◽  
Jie Dong ◽  
Zhe Cai ◽  
...  
2021 ◽  
Vol 22 (8) ◽  
pp. 3970
Author(s):  
Md Razib Hossain ◽  
Tuba M. Ansary ◽  
Mayumi Komine ◽  
Mamitaro Ohtsuki

The production of melanin pigments by melanocytes and their quantity, quality, and distribution play a decisive role in determining human skin, eye, and hair color, and protect the skin from adverse effects of ultraviolet radiation (UVR) and oxidative stress from various environmental pollutants. Melanocytes reside in the basal layer of the interfollicular epidermis and are compensated by melanocyte stem cells in the follicular bulge area. Various stimuli such as eczema, microbial infection, ultraviolet light exposure, mechanical injury, and aging provoke skin inflammation. These acute or chronic inflammatory responses cause inflammatory cytokine production from epidermal keratinocytes as well as dermal fibroblasts and other cells, which in turn stimulate melanocytes, often resulting in skin pigmentation. It is confirmed by some recent studies that several interleukins (ILs) and other inflammatory mediators modulate the proliferation and differentiation of human epidermal melanocytes and also promote or inhibit expression of melanogenesis-related gene expression directly or indirectly, thereby participating in regulation of skin pigmentation. Understanding of mechanisms of skin pigmentation due to inflammation helps to elucidate the relationship between inflammation and skin pigmentation regulation and can guide development of new therapeutic pathways for treating pigmented dermatosis. This review covers the mechanistic aspects of skin pigmentation caused by inflammation.


2021 ◽  
Author(s):  
Natalija Novak ◽  
Heike Weighardt ◽  
Rafael Valdelvira ◽  
Elena Izquierdo ◽  
Irmgard Förster ◽  
...  

2015 ◽  
Vol 165 ◽  
pp. 54-60 ◽  
Author(s):  
Bo-Kyung Park ◽  
Yang-Chun Park ◽  
In Chul Jung ◽  
Seung-Hyung Kim ◽  
Jeong June Choi ◽  
...  

2006 ◽  
Vol 103 (23) ◽  
pp. 8816-8821 ◽  
Author(s):  
M. Terada ◽  
H. Tsutsui ◽  
Y. Imai ◽  
K. Yasuda ◽  
H. Mizutani ◽  
...  

Author(s):  
E. Morita ◽  
H. Takahashi ◽  
H. Niihara ◽  
I. Dekio ◽  
Y. Sumikawa ◽  
...  

2018 ◽  
Vol 138 (5) ◽  
pp. S161
Author(s):  
N. Archer ◽  
S. Lee ◽  
J. Jo ◽  
D. Kim ◽  
R. Ortines ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-5
Author(s):  
Christina Bothou ◽  
Alexis Alexopoulos ◽  
Eleni Dermitzaki ◽  
Kleanthis Kleanthous ◽  
Anastasios Papadimitriou ◽  
...  

Atopic dermatitis (AD) is a chronic inflammatory disease affecting children and adolescence. The traditional therapeutic options for AD, including emollients topically and immune modulatory agents systemically focusing on reducing skin inflammation and restoring the function of the epidermal barrier, are proven ineffective in many cases. Several studies have linked vitamin D supplementation with either a decreased risk to develop AD or a clinical improvement of the symptoms of AD patients. In this report, we present a girl with severe AD who under adequate supplementation with cholecalciferol was treated with calcitriol and subsequently with paricalcitol. She had significant improvement—almost healing of her skin lesions within 2 months, a result sustained for more than 3 years now. Because of hypercalciuria as a side effect from calcitriol therapy, treatment was continued with paricalcitol, a vitamin D analogue used in secondary hyperparathyroidism in chronic kidney disease. Calcitriol therapy may be considered as a safe and efficacious treatment option for patients with severe AD, particularly for those with refractory AD, under monitoring for possible side effects. Treatment with paricalcitol resolves hypercalciuria, is safe, and should be further investigated as an alternative treatment of atopic dermatitis and possibly other diseases of autoimmune origin.


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