Ham NaYeon, Park Minji, Bae Young-An, Yeo Eui-Ju, Jung YunJae
Department of Microbiology, Graduate School of Medicine, Gachon University, Incheon, South Korea.
Department of Health Science and Technology, Gachon Advanced Institute for Health Science & Technology, Gachon University, Incheon, South Korea.
Anim Cells Syst (Seoul). 2025 Jan 18;29(1):100-112. doi: 10.1080/19768354.2025.2451408. eCollection 2025.
Inflammatory bowel disease is a chronic condition characterized by inflammation of the gastrointestinal tract, resulting from an abnormal immune response to normal stimuli, such as food and intestinal flora. Since the etiology of this disease remains largely unknown, murine models induced by the consumption of dextran-sodium sulfate serve as a pivotal tool for studying colon inflammation. In this study, we employed both acute and chronic colitis mouse models induced by varying durations of dextran-sodium sulfate consumption to investigate the pathological and immunologic characteristics throughout the disease course. During the acute phase, activated innate inflammation marked by M1 macrophage infiltration was prominent. In contrast, the chronic phase was characterized by tissue remodeling, with a significant increase in M2 macrophages and lymphocytes. RNA-sequencing revealed genetic changes in acute and chronic colitis, marked by the maintenance of genomic integrity in the acute phase and extracellular matrix dynamics in the chronic phase. These phase-specific alterations reflect the multifaceted physiological processes involved in the initiation and progression of inflammation in the large intestine, underscoring the necessity for distinct experimental approaches for each phase. The findings demonstrate that the factors shaping the large intestinal immune microenvironment change specifically during the acute and chronic phases of experimental inflammatory bowel disease, highlighting the importance of developing therapeutic strategies that align with the disease course.
炎症性肠病是一种以胃肠道炎症为特征的慢性疾病，由对正常刺激（如食物和肠道菌群）的异常免疫反应引起。由于这种疾病的病因在很大程度上仍然未知，食用葡聚糖硫酸钠诱导的小鼠模型成为研究结肠炎症的关键工具。在本研究中，我们使用了通过不同时长食用葡聚糖硫酸钠诱导的急性和慢性结肠炎小鼠模型，以研究整个疾病过程中的病理和免疫特征。在急性期，以M1巨噬细胞浸润为特征的活化先天性炎症较为突出。相比之下，慢性期的特征是组织重塑，M2巨噬细胞和淋巴细胞显著增加。RNA测序揭示了急性和慢性结肠炎中的基因变化，急性期以基因组完整性维持为特征，慢性期以细胞外基质动态变化为特征。这些阶段特异性改变反映了大肠炎症起始和进展过程中涉及的多方面生理过程，强调了针对每个阶段采用不同实验方法的必要性。研究结果表明，在实验性炎症性肠病的急性和慢性阶段，塑造大肠免疫微环境的因素会发生特异性变化，突出了制定与疾病进程相匹配的治疗策略的重要性。
