Ya O Yemchenko, V I Shynkevych, K Ye Ishcheikin, I P Kaidashev
{"title":"PPAR-Gamma 激动剂吡格列酮可减少肥胖银屑病患者的 CD68+ 而非 CD163+ 巨噬细胞真皮浸润","authors":"Ya O Yemchenko, V I Shynkevych, K Ye Ishcheikin, I P Kaidashev","doi":"10.1155/2020/4548012","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Macrophages are of great importance in the development of obesity and psoriasis. Signaling via PPAR-<i>γ</i> in certain macrophage populations is associated with M2-like features and anti-inflammatory profile. In this research, we evaluated the anti-inflammatory action of pioglitazone by the immunohistochemical study of M1 and M2 macrophages in psoriasis-affected skin in obese patients.</p><p><strong>Methods: </strong>We used immunohistochemistry to characterize CD68+ and CD163+ macrophages and pathomorphological description of skin biopsy, obtained from 6 obese psoriatic patients before and after treatment with 15, 30, and 45 mg pioglitazone, once a day during 6 months. Two patients with conventional therapy and without pioglitazone served as control.</p><p><strong>Results: </strong>Generally, CD163+ cell quantities in psoriasis-affected skin significantly dominated over CD68+ before and after all treatment regiments. Among patients who received pioglitazone, some of them clearly responded to treatment from lowest to highest doses by decreasing CD68+ cells. In the group with 30 mg pioglitazone regiment, we detected a significant reduction of CD68+ cells in dermal infiltrates: CI 95% (16-32) before versus CI 95% (2-7) after treatment. Pioglitazone dose escalation led to certain normalization of skin morphology.</p><p><strong>Conclusion: </strong>The immunohistochemical study allows us to show the anti-inflammatory effect of pioglitazone in psoriatic obese patients, which can be mediated by reducing the number of СD68+ macrophages, but not СD163+ macrophages, in the affected dermis.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":null,"pages":null},"PeriodicalIF":3.5000,"publicationDate":"2020-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7211254/pdf/","citationCount":"0","resultStr":"{\"title\":\"PPAR-Gamma Agonist Pioglitazone Reduced CD68+ but Not CD163+ Macrophage Dermal Infiltration in Obese Psoriatic Patients.\",\"authors\":\"Ya O Yemchenko, V I Shynkevych, K Ye Ishcheikin, I P Kaidashev\",\"doi\":\"10.1155/2020/4548012\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Macrophages are of great importance in the development of obesity and psoriasis. Signaling via PPAR-<i>γ</i> in certain macrophage populations is associated with M2-like features and anti-inflammatory profile. In this research, we evaluated the anti-inflammatory action of pioglitazone by the immunohistochemical study of M1 and M2 macrophages in psoriasis-affected skin in obese patients.</p><p><strong>Methods: </strong>We used immunohistochemistry to characterize CD68+ and CD163+ macrophages and pathomorphological description of skin biopsy, obtained from 6 obese psoriatic patients before and after treatment with 15, 30, and 45 mg pioglitazone, once a day during 6 months. Two patients with conventional therapy and without pioglitazone served as control.</p><p><strong>Results: </strong>Generally, CD163+ cell quantities in psoriasis-affected skin significantly dominated over CD68+ before and after all treatment regiments. Among patients who received pioglitazone, some of them clearly responded to treatment from lowest to highest doses by decreasing CD68+ cells. In the group with 30 mg pioglitazone regiment, we detected a significant reduction of CD68+ cells in dermal infiltrates: CI 95% (16-32) before versus CI 95% (2-7) after treatment. 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引用次数: 0
摘要
背景:巨噬细胞在肥胖和银屑病的发病过程中具有重要作用。某些巨噬细胞群通过 PPAR-γ 信号与 M2 类特征和抗炎特征有关。在这项研究中,我们通过对肥胖患者受银屑病影响的皮肤中的M1和M2巨噬细胞进行免疫组化研究,评估了吡格列酮的抗炎作用:我们使用免疫组化方法描述了CD68+和CD163+巨噬细胞的特征,并对6名肥胖银屑病患者在接受15、30和45毫克吡格列酮治疗前后的皮肤活检进行了病理形态学描述。两名接受常规治疗但未服用吡格列酮的患者作为对照:一般来说,在所有治疗方案前后,受银屑病影响的皮肤中 CD163+ 细胞数量明显多于 CD68+。在接受吡格列酮治疗的患者中,部分患者对从最低剂量到最高剂量的治疗有明显反应,CD68+细胞减少。在使用 30 毫克吡格列酮治疗的组别中,我们发现真皮浸润中的 CD68+ 细胞显著减少:治疗前的 CI 95% (16-32) 与治疗后的 CI 95% (2-7)。吡格列酮剂量的增加使皮肤形态趋于正常:通过免疫组化研究,我们可以发现吡格列酮对银屑病肥胖患者有抗炎作用,这种作用可以通过减少受影响的真皮层中СD68+巨噬细胞(而非СD163+巨噬细胞)的数量来实现。
PPAR-Gamma Agonist Pioglitazone Reduced CD68+ but Not CD163+ Macrophage Dermal Infiltration in Obese Psoriatic Patients.
Background: Macrophages are of great importance in the development of obesity and psoriasis. Signaling via PPAR-γ in certain macrophage populations is associated with M2-like features and anti-inflammatory profile. In this research, we evaluated the anti-inflammatory action of pioglitazone by the immunohistochemical study of M1 and M2 macrophages in psoriasis-affected skin in obese patients.
Methods: We used immunohistochemistry to characterize CD68+ and CD163+ macrophages and pathomorphological description of skin biopsy, obtained from 6 obese psoriatic patients before and after treatment with 15, 30, and 45 mg pioglitazone, once a day during 6 months. Two patients with conventional therapy and without pioglitazone served as control.
Results: Generally, CD163+ cell quantities in psoriasis-affected skin significantly dominated over CD68+ before and after all treatment regiments. Among patients who received pioglitazone, some of them clearly responded to treatment from lowest to highest doses by decreasing CD68+ cells. In the group with 30 mg pioglitazone regiment, we detected a significant reduction of CD68+ cells in dermal infiltrates: CI 95% (16-32) before versus CI 95% (2-7) after treatment. Pioglitazone dose escalation led to certain normalization of skin morphology.
Conclusion: The immunohistochemical study allows us to show the anti-inflammatory effect of pioglitazone in psoriatic obese patients, which can be mediated by reducing the number of СD68+ macrophages, but not СD163+ macrophages, in the affected dermis.
期刊介绍:
PPAR Research is a peer-reviewed, Open Access journal that publishes original research and review articles on advances in basic research focusing on mechanisms involved in the activation of peroxisome proliferator-activated receptors (PPARs), as well as their role in the regulation of cellular differentiation, development, energy homeostasis and metabolic function. The journal also welcomes preclinical and clinical trials of drugs that can modulate PPAR activity, with a view to treating chronic diseases and disorders such as dyslipidemia, diabetes, adipocyte differentiation, inflammation, cancer, lung diseases, neurodegenerative disorders, and obesity.