Thymic stromal lymphopoietin (TSLP) is a cytokine that is known to play a role in inflammatory conditions, especially asthma and atopic dermatitis. It is also recognized to be expressed in human adipose tissue. TSLP production from human adipocytes is stimulated by thyroid-stimulating hormone (TSH). This study aimed to identify TSH-dependent signaling routes that regulate TSLP, to determine if TSLP production is stimulated by other cytokines (IL-1β and TNF-α), and to examine if TSLP production depends on the adipose depot. Human abdominal differentiated adipocytes were stimulated with TSH, IL-1β, or TNF-α. Activation of cell signaling kinases was measured by phospho-immunoblot analysis, and TSLP in medium was assessed by ELISA. TSLP responses from abdominal subcutaneous and omental adipocytes were compared. TSH-stimulated TSLP secretion from subcutaneous adipocytes was enhanced by IBMX (raises cAMP levels) and was blocked by UO126 (inhibitor of MEK1/2-ERK1/2). TSLP secretion was stimulated by IL-1β and by TNF-α. SC-514 (inhibitor of IKKβ/NF-κB) only reduced the former. There was no effect of SB203580 (p38 MAPK inhibitor) or SP600125 (JNK inhibitor) on the stimulation by TSH, IL-1β or TNF-α. Interferon-γ inhibited TSLP responses to TSH, IL-1β, and TNF-α; IL-4 only blocked the response to TNFα. Intra-abdominal omental adipocytes also release TSLP in response to TSH, IL-1β, and TNF-α. We conclude TSLP is produced by human differentiated adipocytes derived from subcutaneous or omental depots in response to a variety of agonists. Further studies will be needed to understand what role it may play in adipose biology.

中文翻译：

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人脂肪细胞产生胸腺基质淋巴细胞生成素的调节剂

胸腺基质淋巴细胞生成素 (TSLP) 是一种细胞因子，已知其在炎症状况中发挥作用，尤其是哮喘和特应性皮炎。它也被认为在人类脂肪组织中表达。人类脂肪细胞产生 TSLP 受促甲状腺激素 (TSH) 刺激。本研究旨在确定调节 TSLP 的 TSH 依赖性信号通路，确定 TSLP 的产生是否受到其他细胞因子（IL-1β 和 TNF-α）的刺激，并检查 TSLP 的产生是否依赖于脂肪库。用 TSH、IL-1β 或 TNF-α 刺激人腹部分化的脂肪细胞。通过磷酸化免疫印迹分析测量细胞信号激酶的激活，并通过ELISA评估培养基中的TSLP。比较来自腹部皮下和网膜脂肪细胞的 TSLP 反应。IBMX 可增强皮下脂肪细胞中 TSH 刺激的 TSLP 分泌（提高 cAMP 水平），并被 UO126（MEK1/2-ERK1/2 抑制剂）阻断。IL-1β 和 TNF-α 刺激 TSLP 分泌。SC-514（IKKβ/NF-κB 抑制剂）仅减少了前者。SB203580（p38 MAPK 抑制剂）或 SP600125（JNK 抑制剂）对 TSH、IL-1β 或 TNF-α 的刺激没有影响。干扰素-γ 抑制 TSLP 对 TSH、IL-1β 和 TNF-α 的反应；IL-4 仅阻断对 TNFα 的反应。腹内网膜脂肪细胞也会响应 TSH、IL-1β 和 TNF-α 释放 TSLP。我们得出结论，TSLP 是由来自皮下或网膜贮库的人类分化脂肪细胞对各种激动剂产生反应产生的。需要进一步研究以了解它在脂肪生物学中可能发挥的作用。