纳米硫化铁对小鼠感染性湿疹模型的影响及机制研究

Effect and mechanism of nano-iron sulfide on murine infected eczema

采用2,4-二硝基氯苯(DNCB)对小鼠背部皮肤进行致敏,并加以金黄色葡萄球菌感染,建立小鼠感染性湿疹模型,观察纳米硫化铁对小鼠皮肤损伤的影响,皮肤匀浆培养皮肤损伤菌群数量,皮肤损伤组织病理变化;ELISA法检测小鼠血清中白介素(IL)-10和干扰素(IFN)-γ表达水平,以探讨纳米硫化铁对小鼠感染性湿疹模型的影响及可能机制。结果表明:经DNCB处理并感染金黄色葡萄球菌,小鼠出现红斑、丘疹、水疱、伴有黄色结痂,表明模型建立成功,纳米硫化铁处理后,皮肤损伤明显改善, EASI评分下降;皮肤匀浆培养菌落数明显减少(P<0.01);组织病理为模型组表皮可见明显角化不全伴角化过度,棘层明显增厚,棘细胞间水肿,真皮浅层可见炎症细胞浸润,纳米硫化铁组表皮增厚及炎症细胞浸润较模型组减轻;血清炎症指标,与模型组相比,纳米硫化铁组小鼠血清IL-10表达水平降低(P<0.01),血清IFN-γ水平明显升高(P<0.001)。该研究说明纳米硫化铁对金黄色葡萄球菌有明显抑菌作用,可改善小鼠感染性湿疹模型皮肤炎症,降低炎症因子IL-10水平,促进IFN-γ表达。

Mouse were sensitized by 2,4-dinitrochlorobenzene(DNCB) and innoculated with Staphylococcus aureus to establish a murine infectious eczema. Observe the improvement of nFeS on mouse skin lesions;Count the viable bacteria in mouse skin homogenate liquid cultivation;Observe the histopathological changes of skin lesions by HE staining, and the expression levels of IL-10 and IFN-γ serum were measured by ELISA. To investigate the effect of a novel nanomaterial, nano-iron sulfide(nFeS), on murine infected eczema and underlying mechanism. The mouse treated with DNCB and innoculated with staphylococcus aureus showed obvious erythema, papule, blister, accompanied by yellow scab. It shows that the infected eczema mouse model is established successfully. After treated with nFeS, the skin lesions were improved markedly with decreased EASI scores. The number of bacteria of skin homogenate liquid cultivation decreased significantly(compared with the model group, P<0.01). Histopathological analyses: in model group, hyperkeratosis and parakeratosis and acanthosis, and intercellular edema were observed in the epidermis, inflammatory cells infiltration in the superficial dermis, skin thickening and inflammatory cells infiltration were less in nFeS group than that in model group;Serum inflammatory biomarkers: compared with model group, the expression level of serum IL-10 in nFeS group decreased(P<0.01), while serum IFN-γ increased significantly(P<0.001). Conclusion The nFeS has significant bacteriostatic effect on S.aureus and can ameliorate skin inflammation in mouse model of infectious eczema. The nFeS can down-regulate the serum inflammatory cytokines IL-10, and up-regulated the level of IFN-γ.