Key Laboratory of Medical Science and Laboratory Medicine of Jiangsu Province, School of Medicine, Jiangsu University, 301 Xuefu Road, Zhenjiang, 212013, Jiangsu, People's Republic of China.
Directorate of University Health Services, University of Cape Coast, Cape Coast, Ghana.
J Transl Med. 2021 Jun 10;19(1):254. doi: 10.1186/s12967-021-02922-2.
Recent studies reporting the intricate crosstalk between cellular and molecular mediators and the lymphatic endothelium in the development of inflammatory bowel diseases (IBD) suggest altered inflammatory cell drainage and lymphatic vasculature, implicating the lymphatic system as a player in the occurrence, development, and recurrence of intestinal diseases. This article aims to review recent data on the modulatory functions of cellular and molecular components of the IBD microenvironment on the lymphatic system, particularly lymphangiogenesis. It serves as a promising therapeutic target for IBD management and treatment. The interaction with gut microbiota is also explored.
Evidence shows that cells of the innate and adaptive immune system and certain non-immune cells participate in the complex processes of inflammatory-induced lymphangiogenesis through the secretion of a wide spectrum of molecular factors, which vary greatly among the various cells. Lymphangiogenesis enhances lymphatic fluid drainage, hence reduced infiltration of immunomodulatory cells and associated-inflammatory cytokines. Interestingly, some of the cellular mediators, including mast cells, neutrophils, basophils, monocytes, and lymphatic endothelial cells (LECs), are a source of lymphangiogenic molecules, and a target as they express specific receptors for lymphangiogenic factors.
The effective target of lymphangiogenesis is expected to provide novel therapeutic interventions for intestinal inflammatory conditions, including IBD, through both immune and non-immune cells and based on cellular and molecular mechanisms of lymphangiogenesis that facilitate inflammation resolution.
最近的研究报告表明，细胞和分子介质与炎症性肠病（IBD）中淋巴内皮细胞之间的复杂串扰提示炎症细胞引流和淋巴管系统发生改变，表明淋巴系统在肠道疾病的发生、发展和复发中起作用。本文旨在综述 IBD 微环境中细胞和分子成分对淋巴管系统（特别是淋巴管生成）的调节功能的最新数据。它是 IBD 管理和治疗的有前途的治疗靶点。还探讨了与肠道微生物群的相互作用。
有证据表明，先天和适应性免疫系统的细胞以及某些非免疫细胞通过分泌广泛的分子因子参与炎症诱导的淋巴管生成的复杂过程，而各种细胞之间的分子因子差异很大。淋巴管生成增强了淋巴液的引流，从而减少了免疫调节细胞和相关炎症细胞因子的浸润。有趣的是，一些细胞介质，包括肥大细胞、中性粒细胞、嗜碱性粒细胞、单核细胞和淋巴内皮细胞（LEC），是淋巴管生成分子的来源，也是它们表达特定的淋巴管生成因子受体的靶标。
预期淋巴管生成的有效靶点将通过免疫和非免疫细胞，并基于促进炎症消退的淋巴管生成的细胞和分子机制，为包括 IBD 在内的肠道炎症疾病提供新的治疗干预措施。
