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Immune Response in Atopic Dermatitis

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Dear Colleagues,

The skin is one of the largest immune organs that involve innate and acquired immune systems and thus is able to respond to exogenous stimuli producing large amount of proinflammatory cytokines, resulting in systemic inflammation.

Atopic dermatitis has been regarded as one of the type 2 immune disorders, and lymphocytes produce IL-4 and IL-13 mainly; however, in the actural skin inflammation, type 1 and type 3 cells may intermingle in the lesions. Several studies have shown that severe inflammatory skin disorders are deeply connected to systemic complications such as arteriosclerosis, cardiomyopathy, abnormal fat metabolism, renal sclerosis, and systemic amyloidosis, leading to a concept of inflammatory skin march: intimate relations between skin inflammation and complications. Here, we welcome the clinical evidence and research findings focusing on immunological mechanism, systemic inflammatory changes and systemic organ diseases complicated by atopic dermatitis.

Prof. Dr. Keiichi Yamanaka
Guest Editor

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Keywords

inflammatory skin disease
atopic dermatitis
cytokine
IL-4
IL-13
comorbidities

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Research

16 pages, 3348 KiB

Open AccessArticle

Inflammatory Skin Disease Causes Anxiety Symptoms Leading to an Irreversible Course

by Shohei Iida, Hirotaka Shoji, Fumihiro Kawakita, Takehisa Nakanishi, Yoshiaki Matsushima, Makoto Kondo, Koji Habe, Hidenori Suzuki, Tsuyoshi Miyakawa and Keiichi Yamanaka

Int. J. Mol. Sci. 2023, 24(6), 5942; https://doi.org/10.3390/ijms24065942 - 21 Mar 2023

Cited by 1 | Viewed by 1441

Abstract

Intense itching significantly reduces the quality of life, and atopic dermatitis is associated with psychiatric conditions, such as anxiety and depression. Psoriasis, another inflammatory skin disease, is often complicated by psychiatric symptoms, including depression; however, the pathogenesis of these mediating factors is poorly understood. This study used a spontaneous dermatitis mouse model (KCASP1Tg) and evaluated the psychiatric symptoms. We also used Janus kinase (JAK) inhibitors to manage the behaviors. Gene expression analysis and RT-PCR of the cerebral cortex of KCASP1Tg and wild-type (WT) mice were performed to examine differences in mRNA expression. KCASP1Tg mice had lower activity, higher anxiety-like behavior, and abnormal behavior. The mRNA expression of S100a8 and Lipocalin 2 (Lcn2) in the brain regions was higher in KCASP1Tg mice. Furthermore, IL-1β stimulation increased Lcn2 mRNA expression in astrocyte cultures. KCASP1Tg mice had predominantly elevated plasma Lcn2 compared to WT mice, which improved with JAK inhibition, but behavioral abnormalities in KCASP1Tg mice did not improve, despite JAK inhibition. In summary, our data revealed that Lcn2 is closely associated with anxiety symptoms, but the anxiety and depression symptoms caused by chronic skin inflammation may be irreversible. This study demonstrated that active control of skin inflammation is essential for preventing anxiety. Full article

(This article belongs to the Special Issue Immune Response in Atopic Dermatitis)

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15 pages, 3769 KiB

Open AccessArticle

Arteriosclerosis Derived from Cutaneous Inflammation Is Ameliorated by the Deletion of IL-17A and IL-17F

by Takehisa Nakanishi, Shohei Iida, Junko Maruyama, Hayato Urushima, Masako Ichishi, Yoshiaki Matsushima, Kento Mizutani, Yuichi Nakayama, Kyoko Sugioka, Mai Nishimura, Ai Umaoka, Yoichiro Iwakura, Makoto Kondo, Koji Habe, Daisuke Tsuruta, Osamu Yamamoto, Yasutomo Imai and Keiichi Yamanaka

Int. J. Mol. Sci. 2023, 24(6), 5434; https://doi.org/10.3390/ijms24065434 - 12 Mar 2023

Cited by 3 | Viewed by 1852

Abstract

The skin is one of the major immune organs producing large amounts of proinflammatory and inflammatory cytokines in response to internal or exogenous stimuli, inducing systemic inflammation in various internal organs. In recent years, organ damage associated with inflammatory skin diseases such as psoriasis and atopic dermatitis has received increasing attention, and vascular disorder such as arteriosclerosis is one of the serious complications of chronic inflammatory skin diseases. However, the detailed mechanism of arteriosclerosis in dermatitis and the role of cytokines have not been clarified so far. In the current study, using a spontaneous dermatitis model, we investigated the pathophysiology of arteriosclerosis and the treatment option for inflammatory skin conditions. We employed spontaneous dermatitis model mice overexpressing human caspase-1 in the epidermal keratinocyte (Kcasp1Tg). The thoracic and abdominal aorta was investigated histologically. GeneChip and RT-PCR analysis were performed to measure the changes in mRNA levels in the aorta. To elucidate the direct effect on the artery by major inflammatory cytokines, endothelial cells, vascular smooth muscle cells, and fibroblast cells were co-cultured with several cytokines, and mRNA expression levels were measured. In order to observe the efficacy of IL-17A/F in arteriosclerosis, cross-mating with IL-17A, IL-17F, and IL-17A/F deficient mice was performed. Finally, we also measured snap tension in the abdominal aorta in WT, Kcasp1Tg, and IL17A/F-deficient mice. Kcasp1Tg showed a decrease in the diameter of the abdominal aorta compared to wild-type mice. mRNA levels for six genes including Apol11b, Camp, Chil3, S100a8, S100a9, and Spta1 were increased in the abdominal aorta of Kcasp1Tg. Some of the above mRNA levels were also increased in the co-culture with major inflammatory cytokines, IL-17A/F, IL-1β, and TNF-α. Dermatitis improved and mRNA levels were partially ameliorated in Kcasp1Tg with IL-17A/F deletion. Arterial fragility was also evidenced in the inflammatory model, but arterial flexibility was revealed in the IL-17A/F deletion model. Severe dermatitis is closely related to secondary arteriosclerosis caused by the persistent release of inflammatory cytokines. The results also proved that treatment against IL-17A and F may ameliorate arteriosclerosis. Full article

(This article belongs to the Special Issue Immune Response in Atopic Dermatitis)

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