PDF(Pubmed)
Abstract：
UNASSIGNED: Atopic dermatitis (AD) is a chronic, non-infectious inflammatory dermatosis. Chloroquine (CQ) has long been proven to possess anti-inflammatory properties.
UNASSIGNED: This paper aims to investigate the impact of CQ on type 2 inflammatory response in MC903-induced AD mice.
UNASSIGNED: An AD mouse model was established via MC903 induction. After CQ treatment, AD mice were intraperitoneally injected with polyinosinic: polycyclic acid [poly (I:C)] or Nigericin. Dermatitis severity was scored, and the thickness of the left ear was measured. The pathological changes in mouse skin tissues were observed by H&E staining. The number of mast cells was counted via TB staining. The content of peripheral blood T-helper 2 (Th2) cells and levels of immunoglobulin E (IgE), thymic stromal-derived lymphopoietin (TSLP), interleukin (IL)-4, IL-13, interferon (IFN)-γ, IL-1β, and IL-18 were assessed by flow cytometry and ELISA. The levels of toll-like receptor 3 (TLR3), NLRP3, ASC, and cleaved caspase-1 proteins in skin tissues were determined by Western blot.
UNASSIGNED: CQ treatment abated dermatitis severity and left ear thickness in AD mice, alleviated skin damage, reduced mast cell number, diminished IgE, TSLP, IL-4, and IL-13 levels, and peripheral blood Th2 cell content, with no significant changes in IFN-γ level. CQ alleviated type 2 inflammatory response in AD mice by inhibiting the activation of TLR3. CQ suppressed NLRP3 inflammasome activation. Activating TLR3/NLRP3 annulled CQ-mediated alleviation on type 2 inflammatory response in AD mice.
UNASSIGNED: CQ alleviated type 2 inflammatory response in AD mice by inhibiting TLR3 activation and NLRP3 inflammasome activation.
UNASSIGNED: This paper aims to investigate the impact of CQ on type 2 inflammatory response in MC903-induced AD mice.
UNASSIGNED: An AD mouse model was established via MC903 induction. After CQ treatment, AD mice were intraperitoneally injected with polyinosinic: polycyclic acid [poly (I:C)] or Nigericin. Dermatitis severity was scored, and the thickness of the left ear was measured. The pathological changes in mouse skin tissues were observed by H&E staining. The number of mast cells was counted via TB staining. The content of peripheral blood T-helper 2 (Th2) cells and levels of immunoglobulin E (IgE), thymic stromal-derived lymphopoietin (TSLP), interleukin (IL)-4, IL-13, interferon (IFN)-γ, IL-1β, and IL-18 were assessed by flow cytometry and ELISA. The levels of toll-like receptor 3 (TLR3), NLRP3, ASC, and cleaved caspase-1 proteins in skin tissues were determined by Western blot.
UNASSIGNED: CQ treatment abated dermatitis severity and left ear thickness in AD mice, alleviated skin damage, reduced mast cell number, diminished IgE, TSLP, IL-4, and IL-13 levels, and peripheral blood Th2 cell content, with no significant changes in IFN-γ level. CQ alleviated type 2 inflammatory response in AD mice by inhibiting the activation of TLR3. CQ suppressed NLRP3 inflammasome activation. Activating TLR3/NLRP3 annulled CQ-mediated alleviation on type 2 inflammatory response in AD mice.
UNASSIGNED: CQ alleviated type 2 inflammatory response in AD mice by inhibiting TLR3 activation and NLRP3 inflammasome activation.
摘要：
■特应性皮炎（AD）是一种慢性，非感染性炎症性皮肤病。氯喹（CQ）早已被证明具有抗炎特性。
■本文旨在研究CQ对MC903诱导的AD小鼠2型炎症反应的影响。
■通过MC903诱导建立AD小鼠模型。CQ治疗后,将AD小鼠腹膜内注射聚肌苷酸:多环酸[聚(I:C)]或Nigericin。对皮炎严重程度进行评分，测量左耳的厚度。通过H&E染色观察小鼠皮肤组织的病理变化。通过TB染色计数肥大细胞的数量。外周血辅助性T细胞2(Th2)含量及免疫球蛋白E(IgE)水平,胸腺基质来源的淋巴细胞生成素（TSLP），白细胞介素（IL）-4，IL-13，干扰素（IFN）-γ，IL-1β,通过流式细胞术和ELISA评估IL-18。Toll样受体3（TLR3）的水平，NLRP3,ASC,通过Westernblot测定皮肤组织中裂解的caspase-1蛋白。
■CQ治疗减轻了AD小鼠的皮炎严重程度和左耳厚度，减轻皮肤损伤，肥大细胞数量减少,IgE减少,TSLP,IL-4和IL-13水平，和外周血Th2细胞含量，IFN-γ水平无显著变化。CQ通过抑制TLR3的激活减轻AD小鼠2型炎症反应。CQ抑制NLRP3炎性体激活。激活TLR3/NLRP3使CQ介导的对AD小鼠2型炎症反应的缓解无效。
■CQ通过抑制TLR3激活和NLRP3炎性体激活减轻AD小鼠2型炎症反应。
■本文旨在研究CQ对MC903诱导的AD小鼠2型炎症反应的影响。
■通过MC903诱导建立AD小鼠模型。CQ治疗后,将AD小鼠腹膜内注射聚肌苷酸:多环酸[聚(I:C)]或Nigericin。对皮炎严重程度进行评分，测量左耳的厚度。通过H&E染色观察小鼠皮肤组织的病理变化。通过TB染色计数肥大细胞的数量。外周血辅助性T细胞2(Th2)含量及免疫球蛋白E(IgE)水平,胸腺基质来源的淋巴细胞生成素（TSLP），白细胞介素（IL）-4，IL-13，干扰素（IFN）-γ，IL-1β,通过流式细胞术和ELISA评估IL-18。Toll样受体3（TLR3）的水平，NLRP3,ASC,通过Westernblot测定皮肤组织中裂解的caspase-1蛋白。
■CQ治疗减轻了AD小鼠的皮炎严重程度和左耳厚度，减轻皮肤损伤，肥大细胞数量减少,IgE减少,TSLP,IL-4和IL-13水平，和外周血Th2细胞含量，IFN-γ水平无显著变化。CQ通过抑制TLR3的激活减轻AD小鼠2型炎症反应。CQ抑制NLRP3炎性体激活。激活TLR3/NLRP3使CQ介导的对AD小鼠2型炎症反应的缓解无效。
■CQ通过抑制TLR3激活和NLRP3炎性体激活减轻AD小鼠2型炎症反应。
