Interleukin (IL)-17A and IL-22-producing neutrophils in psoriatic skin

Dyring‐Andersen, Beatrice; Honoré, T. Velte; Madelung, Ann Brinch; Bzorek, Michael; Simonsen, Stine; Clemmensen, Stine Novrup; Clark, Rachael A.; Borregaard, Niels; Skov, Lone

doi:10.1111/bjd.15533

Cited by 42 publications

(50 citation statements)

References 17 publications

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“…Neutrophils play an important role in the pathogenesis of psoriasis by migrating to the epidermis to form Munro's micro‐abscesses . Activated neutrophils release pro‐inflammatory cytokines such as IL‐17, AMPs and proteases and are origin of IL‐17 in psoriatic skin . We document that neutrophil infiltration was significantly increased in RD‐IMQ mice and that HFD mice manifested the high infiltration by neutrophils but not macrophages.…”

Section: Discussionmentioning

confidence: 75%

“…[50] Activated neutrophils release pro-inflammatory cytokines such as IL-17, AMPs and proteases and are origin of IL-17 in psoriatic skin. [51,52] We document that neutrophil infiltration was significantly increased in RD-IMQ mice and that HFD mice manifested the high infiltration by neutrophils but not macrophages. Neutrophils activate inflammasome by stimulation such as LPS, bacteria and urate crystal.…”

Section: Discussionmentioning

confidence: 97%

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High‐fat diet exacerbates imiquimod‐induced psoriasis‐like dermatitis in mice

Higashi

Yamakuchi

Fukushige

et al. 2018

Experimental Dermatology

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Psoriasis, a chronic inflammatory skin disease, is closely related to systemic metabolism. An elevated body mass index (BMI) is a risk factor for psoriasis; inflammasomes are activated by adipose tissue macrophages in obese subjects. We hypothesized that hyperlipidaemia is involved in the pathogenesis of psoriasis and examined the role of a high-fat diet (HFD) in the development of psoriasis in imiquimod (IMQ)-treated mice. The body weight and serum level of cholesterol were significantly higher in mice fed an HFD than in a regular diet (RD). HFD mice had higher psoriasis skin scores, and the number of neutrophils infiltrating into the lesional skin was elevated. IL-17A mRNA expression was significantly increased in the skin of IMQ-treated HFD mice; the expression of IL-22, IL-23 and TNF-α mRNA was not enhanced. Caspase-1 and IL-1β were activated in the skin of IMQ-treated HFD mice, and their serum level of IL-17A, TNF-α and IL-1β was significantly upregulated. Our findings strongly suggest that hyperlipidaemia is involved in the development and progression of psoriasis via systemic inflammation and inflammasome activation.

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Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 97%

High‐fat diet exacerbates imiquimod‐induced psoriasis‐like dermatitis in mice

Higashi

Yamakuchi

Fukushige

et al. 2018

Experimental Dermatology

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“…These results indicate the importance of the secreted cytokine environment that surrounds vitiliginous melanocytes with regard to vitiligo etiology. In the epidermis, IL-17 can be secreted as a homodimer and binds to its receptor, IL-17R, on keratinocytes, which leads to increased production of the cytokines, IL-1b, IL-6, IL-8, and TNF-a (39,40). Stimulation of keratinocytes with IL-17 also up-regulates gene expression of human b-defensin 2 and other antimicrobial peptides and chemokine CCL20 (41).…”

Section: Discussionmentioning

confidence: 99%

IL‐17 induces cellular stress microenvironment of melanocytes to promote autophagic cell apoptosis in vitiligo

Zhou

Dong

et al. 2018

FASEB j.

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Vitiligo is a depigmentary disorder that develops as a result of the progressive disappearance of epidermal melanocytes. Stress can precipitate or exacerbate a skin disease through psychosomatic mechanisms. Stress exposure induces vitiligo-like symptoms in mice, as cellular damage to melanocytes causes synthetic pigment loss. Stress also increases IL-17, IL-1β, and antimelanocyte IgG in model mouse serum. Up-regulation of the IL-1β transcript in patients suggests its possible role in autoimmune pathogenesis of vitiligo. We demonstrate that IL-17 promoted IL-1β secretion from keratinocytes. Mitochondrial dysfunction, which can induce the excessive production of reactive oxygen species (ROS), is emerging as a mechanism that underlies various inflammatory and autoimmune diseases. In this study, we demonstrate that IL-17 inhibits melanogenesis of zebrafish, normal human epidermal melanocytes, and B16F10 cells. IL-17 increased mitochondrial dysfunction and ROS accumulation, which was related to autophagy induction. Autophagy is needed for autophagic apoptosis of B16F10 cells induced by IL-17. To inhibit ROS generation, B16F10 cells were pretreated with N-acetyl-l-cysteine (NAC), which inhibited autophagy. 3-Methyladenine (3-MA) also had an inhibiting effect on autophagy. NAC or 3-MA pretreatments inhibited IL-17-mediated cell apoptosis. In summary, IL-17 induces the cellular stress microenvironment in melanocytes to promote autophagic cell apoptosis in vitiligo.-Zhou, J., An, X., Dong, J., Wang, Y., Zhong, H., Duan, L., Ling, J., Ping, F., Shang, J. IL-17 induces cellular stress microenvironment of melanocytes to promote autophagic cell apoptosis in vitiligo.

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“…Since studies reporting neutrophil positivity to IL‐17A continue to be published, ignoring either the previously mentioned information, or the few works showing the contrary, recently we decided to perform additional investigations . Using multiple methodological approaches (RT‐qPCR, ChIP‐seq, ELISA, intracellular staining and immunoblotting), we could confirm that highly purified populations of human neutrophils, either resting, or activated by a variety of stimulatory conditions, such as TLR and dectin ligands, fungal PAMPs and cytokines, including 20 μg/mL IL‐6 plus 2 μg/mL IL‐23, neither express IL‐17A, IL‐17F, IL‐17B, IL‐17C, IL‐17D and IL‐17E mRNA, nor produce IL‐17A, IL‐17F, IL‐17A/F and IL‐17B in vitro .…”

Section: The Case Of Il‐17 Expression In Human Neutrophilsmentioning

confidence: 98%

“…7 Moreover, immunoprecipitation experiments followed by mass spectrometry have also uncovered that both AF-317-NA and #41802 antibodies actually recognize several proteins expressed in the granules and cytoskeleton of neutrophils, while other anti-human IL-17A antibodies (sc-6077) were found to non-specifically recognize multiple proteins in immunoblotting experiments of neutrophil lysates. 7 Since studies reporting neutrophil positivity to IL-17A continue to be published, 40,41,[43][44][45][46][47][48][49][50][51][52][53] ignoring either the previously mentioned information, or the few works showing the contrary, 7,54-57 recently we decided to perform additional investigations. 9 Using multiple methodological approaches (RT-qPCR, ChIP-seq, ELISA, intracellular staining and immunoblotting), we could confirm that highly purified populations of human neutrophils, either resting, or activated by a variety of stimulatory conditions, such as TLR and dectin ligands, fungal PAMPs and cytokines, including 20 lg/mL IL-6 plus 2 lg/mL IL-23, neither express IL-17A, IL-17F, IL-17B, IL-17C, IL-17D and IL-17E mRNA, nor produce IL-17A, IL-17F, IL-17A/F and IL-17B in vitro.…”

Section: Expression In Human Neutrophilsmentioning

confidence: 99%

Cytokine production by human neutrophils: Revisiting the “dark side of the moon”

Tamassia

Bianchetto-Aguilera

Arruda‐Silva

et al. 2018

Eur J Clin Investigation

121

118

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Polymorphonuclear neutrophils are the most numerous leucocytes present in human blood, and function as crucial players in innate immune responses. Neutrophils are indispensable for the defence towards microbes, as they effectively counter them by releasing toxic enzymes, by synthetizing reactive oxygen species and by producing inflammatory mediators. Interestingly, recent findings have highlighted an important role of neutrophils also as promoters of the resolution of inflammation process, indicating that their biological functions go well beyond simple pathogen killing. Consistently, data from the last decades have highlighted that neutrophils may even contribute to the development of adaptive immunity by performing previously unanticipated functions, including the capacity to extend their survival, directly interact with other leucocytes or cell types, and produce and release a variety of cytokines. In this article, we will summarize the main features of, as well as emphasize some important concepts on, the production of cytokines by human neutrophils.

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Interleukin (IL)-17A and IL-22-producing neutrophils in psoriatic skin

Cited by 42 publications

References 17 publications

High‐fat diet exacerbates imiquimod‐induced psoriasis‐like dermatitis in mice

High‐fat diet exacerbates imiquimod‐induced psoriasis‐like dermatitis in mice

IL‐17 induces cellular stress microenvironment of melanocytes to promote autophagic cell apoptosis in vitiligo

Cytokine production by human neutrophils: Revisiting the “dark side of the moon”

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