The mouse model of 2,4-dinitrochlorbenzene (DNCB)-induced human-like atopic dermatitis (hlAD) has been widely used to test novel treatment strategies and compounds. However, the study designs and methods are highly diverse, presenting different hlAD disease patterns that occur after sensitization and repeated challenge with DNCB on dorsal skin. In addition, there is a lack of information about the progression of the disease during the experiment and the achieved pheno- and endotypes, especially at the timepoint when therapeutic treatment is initiated. We here examine hlAD in a DNCB-induced BALB/cJRj model at different timepoints: (i) before starting treatment with dexamethasone, representing a standard drug control (day 12) and (ii) at the end of the experiment (day 22). Both timepoints display typical AD-associated characteristics: skin thickening, spongiosis, hyper- and parakeratosis, altered cytokine and gene expression, increased lipid mediator formation, barrier protein and antimicrobial peptide abnormalities, as well as lymphoid organ hypertrophy. Increased mast cell infiltration into the skin and elevated immunoglobulin E plasma concentrations indicate a type I allergy response. The DNCB-treated skin showed an extrinsic moderate sub-acute hlAD lesion at day 12 and an extrinsic mild sub-acute to chronic pheno- and endotype at day 22 with a dominating Th2 response. A dependency of the filaggrin formation and expression in correlation to the disease severity in the DNCB-treated skin was found. In conclusion, our study reveals a detailed classification of a hlAD at two timepoints with different inflammatory skin conditions and pheno- and endotypes, thereby providing a better understanding of the DNCB-induced hlAD model in BALB/cJRj mice.

2,4-二硝基氯苯 (DNCB) 诱导的类人特应性皮炎 (hlAD) 小鼠模型已广泛用于测试新型治疗策略和化合物。然而，研究设计和方法高度多样化，呈现出在背部皮肤致敏和重复使用 DNCB 攻击后发生的不同 hlAD 疾病模式。此外，缺乏有关实验过程中疾病进展以及所达到的表型和内型的信息，特别是在开始治疗时的时间点。我们在这里在不同时间点检查 DNCB 诱导的 BALB/cJRj 模型中的 hlAD：(i) 开始用地塞米松治疗之前，代表标准药物对照（第 12 天）和 (ii) 实验结束时（第 22 天）。两个时间点都显示出典型的 AD 相关特征：皮肤增厚、海绵组织增生、角化过度和角化不全、细胞因子和基因表达改变、脂质介质形成增加、屏障蛋白和抗菌肽异常以及淋巴器官肥大。皮肤肥大细胞浸润增加和免疫球蛋白 E 血浆浓度升高表明 I 型过敏反应。DNCB处理的皮肤在第12天显示出外在中度亚急性hlAD病变，在第22天显示出外在轻度亚急性至慢性表型和内型，并具有主导的Th2反应。在 DNCB 处理的皮肤中，发现丝聚合蛋白的形成和表达与疾病严重程度相关。总之，我们的研究揭示了具有不同炎症皮肤状况以及表型和内型的两个时间点的 hlAD 的详细分类，从而更好地了解 DNCB 诱导的 BALB/cJRj 小鼠中的 hlAD 模型。