Papaccio G
Institute of Anatomy, 2nd University of Naples, Italy.
Histol Histopathol. 1993 Oct;8(4):751-9.
Type 1 diabetes is characterized by a mononuclear infiltration, commonly called "insulitis". The cells that constitute the insulitis are mainly monocytes that are recruited from extra-islet areas and arrive at the islet site via the vascular system. Infiltrating cells must then pass across the endothelia to gain access to the islet parenchyma. The anatomy and physiology of the islet microvasculature shows that islet B cells are firstly perfused and influence both endocrine non-B islet cells and peri-insular exocrine cells. The low dose streptozocin (LDS) treatment is able to induce, other than a monocyte/macrophage recruitment and activation, islet vascular alterations, mainly at the level of post-capillary venules encircling the islets of Langerhans and a concomitant fall in Superoxide-dismutase (SOD) (the first cellular defence against free radicals) activity. These findings, together with the increase in vascular permeability and the morphological evidence of areas of oedema formation within the islets, have raised the interest in the "microvascular" approach to this disease. Actually the reduction in B-cell perfusion and the concomitant attack by phagocytes with a fall in SOD activity should be considered as events that are linked to each other. On the other hand both macrophages and endothelia are able to produce free radicals and, in particular, nitric oxide. This confirms that the islet vascular system seems to be involved in early insulitis and B-cell lysis.
1型糖尿病的特征是单核细胞浸润，通常称为“胰岛炎”。构成胰岛炎的细胞主要是单核细胞，这些单核细胞从胰岛外区域募集，通过血管系统到达胰岛部位。浸润细胞随后必须穿过内皮细胞才能进入胰岛实质。胰岛微血管的解剖学和生理学表明，胰岛B细胞首先得到灌注，并影响内分泌性非B胰岛细胞和胰岛周围的外分泌细胞。低剂量链脲佐菌素（LDS）治疗除了能够诱导单核细胞/巨噬细胞募集和激活外，还能引起胰岛血管改变，主要发生在环绕胰岛的毛细血管后微静脉水平，同时超氧化物歧化酶（SOD）（细胞对抗自由基的第一道防线）活性下降。这些发现，连同血管通透性增加以及胰岛内出现水肿区域的形态学证据，引发了对该疾病“微血管”研究方法的兴趣。实际上，B细胞灌注减少以及吞噬细胞的伴随攻击导致SOD活性下降，应被视为相互关联的事件。另一方面，巨噬细胞和内皮细胞都能够产生自由基，尤其是一氧化氮。这证实胰岛血管系统似乎参与了早期胰岛炎和B细胞溶解。
