Losartan ointment attenuates imiquimod-induced psoriasis-like inflammation

Zeini, Maryam Shokrian; Haddadi, Nazgol‐Sadat; Shayan, Maryam; Zeini, Mohadese Shokrian; Kazemi, Kiarash; Solaimanian, Shahabaddin; Abdollahifar, Mohammad‐Amin; Hedayatyanfard, Keshvad; Dehpour, Ahmad Reza

doi:10.1016/j.intimp.2021.108160

Cited by 17 publications

(11 citation statements)

References 20 publications

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“…Particularly, Shokrian Zeini et al evaluated the efficacy of losartan ointment on imiquimod-induced inflammation in mice, a model that simulates the features of psoriatic inflammation in humans by inducing an IL-17/IL-23-dependent skin inflammation with erythematous plaques, hyperkeratosis, increasing skin thickness, and significant lymphocytic and neutrophilic infiltrates. 11 The mechanisms underlying EDE induced by biologic therapies are unclear. An imbalance in the Th1/Th17/Th2 immune response has been described in psoriasis and AD, with Th1 and Th17 being more prominent in psoriasis and Th2 more prominent in AD.…”

Section: Discussionmentioning

confidence: 99%

Eczematous drug eruption in patients with psoriasis under anti‐interleukin‐17A: does interleukin‐22 play a key role?

Megna

Caiazzo

Parisi

et al. 2022

Clin Experimental Derm

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Summary Background Eczematous drug eruption (EDE) is a spongiotic skin reaction in response to systemic medications. To date, EDE has been described in patients treated with anti‐interleukin (IL)‐17A monoclonal antibodies with a prevalence of 2.2%–12.1%. Aim To describe the clinical and histological features and the skin cytokine milieu in patients with EDE induced by anti‐IL‐17A biologics. Methods This was a prospective study, enrolling patients with psoriasis who developed EDE during treatment with two anti‐IL‐17 biologics, ixekizumab and secukinumab, from June 2019 to April 2021. Skin biopsies were taken from all patients: a 5‐mm lesional biopsy (LB) and a 3‐mm nonlesional biopsy (NLB). The LB sample was split into two parts, one for histological examination and the other for cytokine profile evaluation. Results During the study period, treatment with an anti‐IL‐17A drug was given to 289 patients of whom 8 (2.8%) developed EDE during the treatment. Histopathological evaluation suggested a diagnosis of spongiotic dermatitis in all eight patients. Cytokine gene expression showed a predominance of T helper (Th)2/Th22 cytokines in EDE lesions with a large increase in IL‐4, IL‐22 and S100A7 levels in both LB and NLB samples compared with healthy skin. IL‐4, IL‐22 and S100A7 were significantly higher in LB compared with NLB samples. IL‐26 levels were also significantly increased in both LB and NLB compared with healthy skin, whereas low levels of IL‐23A were found in both LB and NLB. Conclusion Eczematous drug eruption skin lesions have mainly Th2/Th22 features, with IL‐22 playing a major role in their pathogenesis. EDE seems to be the result of an imbalance towards a Th2/Th22 response, secondary to the blockade of IL‐17A activity.

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Section: Discussionmentioning

confidence: 99%

Eczematous drug eruption in patients with psoriasis under anti‐interleukin‐17A: does interleukin‐22 play a key role?

Megna

Caiazzo

Parisi

et al. 2022

Clin Experimental Derm

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“…To obtain the Baker score, a scoring system for the histological characteristic of psoriasis, at least 10 fields randomly selected were independently examined under the microscope (Nikon, Tokyo, Japan) at a magnification of ×200. The stander of Baker score was the same as previously described …”

Section: Methodsmentioning

confidence: 99%

Tumor-Derived PD-L1⁺ Exosomes with Natural Inflammation Tropism for Psoriasis-Targeted Treatment

et al. 2023

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Background: Psoriasis is a chronic and readily recurrent in ammatory skin disease. To date, there is no cure for psoriasis and signi cant challenges remain in developing more safe and e cacious novel targeted therapies. Psoriasis is characterized by abnormal activation of the immune system, and hyperproliferation and aberrant differentiation of keratinocytes. Psoriatic keratinocytes death is also recently recognized as a major ampli er to the initiation of in ammatory cascade. Given that both keratinocytes and immune cells express high PD-1 in psoriasis, which imply PD-1 as a potential therapeutic target for psoriasis. Here, we developed a well-structured pristimerin nanodot-loaded PD-L1 positive exosome derived from tumor cells (Pri@exo) and elucidated their targeting therapeutic effects.Results: The Pri@exo displays strong cellular uptake and intracellular retention in active CD4 + T cells and HaCaT keratinocytes, suggesting the PD-1 + cells targeting capacity of Pri@exo. Remarkably, Pri@exo signi cantly and safely reversed imiquimod (IMQ)-induced psoriasis in mice, indicated by reducing epidermal thickness, decreasing plaque formation, and over-activating in ammation since it targeted both CD4 + T cells and keratinocytes gathering around the lesion. The increasing in ammatory cytokine excretion of CD4 + T cells in psoriasis was suppressed by Pri@exo. Besides, Pri@exo treatment alleviated ferroptosis-related changes in psoriatic skin, thereby dampening excessive in ammation and, in turn, decreasing the abnormal proliferation of keratinocytes in psoriatic lesions.Conclusion: This tumor-derived PD-L1 + exosomes has a natural in ammatory tropism and excellent antiin ammatory effect, and able to act as a bio-inspired nanocarrier for various therapeutic agents to optimized in ammatory disease therapy.

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“…The standard of Baker's score was the same as previously described. [31] Immunohistochemistry: The 4 μm paraffin skin sections were blocked with 5% BSA for one h and incubated with rabbit anti-CD3 antibody (Servicebio, GB11014, 1:100), rabbit anti-Ly6G antibody (Servicebio, GB11229, 1:100), rabbit anti-CD11c antibody (Servicebio, GB11059, 1:100), rabbit anti-Proliferating cell nuclear antigen (PCNA) antibody (Servicebio, GB11010, 1:100), rabbit anti-Ki67 antibody (Servicebio, GB111141, 1:100), and rabbit anti-MMP9 antibody (Servicebio, GB11132, 1:100) at 4 °C overnight. After washing three times with PBS, the slides were stained with a goat antirabbit IgG secondary antibody rabbit for 50 min at 37 °C.…”

Section: Methodsmentioning

confidence: 99%

Microneedles Loaded with Dexamethasone and Epigallocatechin‐3‐gallate Reverse the Imbalance of Subcutaneous Immune Homeostasis for the Treatment of Psoriasis

Jia,

Yang,

Hong

et al. 2023

Advanced Therapeutics

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Maintaining the homeostasis of the skin's immune microenvironment is crucial for skin's health. In inflammatory skin conditions (like psoriasis), the immune microenvironment is dysregulated, including ROS accumulation and T cell overactivation. In addition to promoting inflammation and excessive keratinocyte proliferation, ROS upregulation in psoriasis also induces glucocorticoid resistance, which poses a significant challenge to the effectiveness of glucocorticoid treatment (e.g., dexamethasone) in psoriasis. To conquer this problem, we used epigallocatechin‐3‐gallate (EGCG) to eliminate ROS production in psoriasis. Application of EGCG reduced ROS levels and improved the anti‐psoriasis effect of Dexamethasone (Dex) in vitro. Benefiting from the unique characteristics of microneedle for transdermal drug delivery, we construct a dissolvable microneedle (MN) patch containing EGCG and Dex (DEX/EGCG‐MN), which can directly codelivery the two elements to the lesion area without stratum corneum barrier. Our MN alleviates psoriasis‐like manifestations in imiquimod (IMQ)‐induced psoriasis mouse model, indicated by epidermal thickness and dorsal skin signs. Besides, DEX/EGCG‐MN corrected the disorder of immune cells, including innate and acquired immune cells. As a result, it mediates the balance in the skin's immune microenvironment. Meanwhile, our MN also ameliorated the hyperproliferation of keratinocytes in psoriatic lesions. We believe this approach may offer insights for further developing anti‐psoriasis assays.This article is protected by copyright. All rights reserved

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Losartan ointment attenuates imiquimod-induced psoriasis-like inflammation

Cited by 17 publications

References 20 publications

Eczematous drug eruption in patients with psoriasis under anti‐interleukin‐17A: does interleukin‐22 play a key role?

Eczematous drug eruption in patients with psoriasis under anti‐interleukin‐17A: does interleukin‐22 play a key role?

Tumor-Derived PD-L1⁺ Exosomes with Natural Inflammation Tropism for Psoriasis-Targeted Treatment

Microneedles Loaded with Dexamethasone and Epigallocatechin‐3‐gallate Reverse the Imbalance of Subcutaneous Immune Homeostasis for the Treatment of Psoriasis

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Losartan ointment attenuates imiquimod-induced psoriasis-like inflammation

Cited by 17 publications

References 20 publications

Eczematous drug eruption in patients with psoriasis under anti‐interleukin‐17A: does interleukin‐22 play a key role?

Eczematous drug eruption in patients with psoriasis under anti‐interleukin‐17A: does interleukin‐22 play a key role?

Tumor-Derived PD-L1+ Exosomes with Natural Inflammation Tropism for Psoriasis-Targeted Treatment

Microneedles Loaded with Dexamethasone and Epigallocatechin‐3‐gallate Reverse the Imbalance of Subcutaneous Immune Homeostasis for the Treatment of Psoriasis

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Product

Resources

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Tumor-Derived PD-L1⁺ Exosomes with Natural Inflammation Tropism for Psoriasis-Targeted Treatment