Nabi A H M Nurun, Islam Laila N, Rahman Mohammad Mahfuzur, Biswas Kazal Boron
Department of Biochemistry and Molecular Biology, University of Dhaka, Dhaka-1000, Bangladesh.
J Biochem Mol Biol. 2005 Nov 30;38(6):661-7. doi: 10.5483/bmbrep.2005.38.6.661.
Since conflicting results have been reported on non-specific immune response in type 1 diabetes, this study evaluates polymorphonuclear neutrophil (PMN) functions in the infection free Long Evan diabetic rats (type 1) by using tests that include: polarization assay, phagocytosis of baker's yeasts (Saccharomyces cerevisiae) and nitroblue tetrazolium (NBT) dye reduction. Polarization assay showed that neutrophils from diabetic rats were significantly activated at the basal level compared to those from the controls (p < 0.001). After PMN activation with N-formylmethionyl-leucyl-phenylalanine (FMLP), control neutrophils were found to be more polarized than those of the diabetic neutrophils and the highest proportions of polarization were found to be 67 % and 57 % at 10(-7) M FMLP, respectively. In the resting state, neutrophils from the diabetic rats reduced significantly more NBT dye than that of the controls (p < 0.001). The percentages of phagocytosis of opsonized yeast cells by the neutrophils from control and diabetic rats were 87 % and 61 %, respectively and the difference was statistically significant (p < 0.001). Evaluation of the phagocytic efficiency of PMNs revealed that control neutrophils could phagocytose 381 +/- 17 whereas those from the diabetic rats phagocytosed 282 +/- 16 yeast cells, and the efficiency of phagocytosis varied significantly (p < 0.001). Further, both the percentages of phagocytosis and the efficiency of phagocytosis by the diabetic neutrophils were inversely related with the levels of their corresponding plasma glucose (p = 0.02; r = -0.498 and p < 0.05; r = -0.43, respectively), which indicated that increased plasma glucose reduced the phagocytic ability of neutrophils. Such relationship was not observed with the control neutrophils. These data clearly indicate that PMN functions are altered in the streptozotocin (STZ)-induced diabetic rats, and hyperglycemia may be the cause for the impairment of their functions leading to many infectious episodes.
由于关于1型糖尿病非特异性免疫反应的报道结果相互矛盾，本研究通过包括极化测定、吞噬面包酵母（酿酒酵母）和硝基蓝四氮唑（NBT）染料还原试验，评估无感染的长 Evans 糖尿病大鼠（1型）中性粒细胞（PMN）的功能。极化测定显示，与对照组相比，糖尿病大鼠的中性粒细胞在基础水平上显著激活（p < 0.001）。在用N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸（FMLP）激活PMN后，发现对照中性粒细胞比糖尿病中性粒细胞更易极化，在10(-7) M FMLP时，最高极化比例分别为67%和57%。在静息状态下，糖尿病大鼠的中性粒细胞还原NBT染料的量明显多于对照组（p < 0.001）。对照和糖尿病大鼠中性粒细胞对调理酵母细胞的吞噬百分比分别为87%和61%，差异具有统计学意义（p < 0.001）。对PMN吞噬效率的评估显示，对照中性粒细胞可吞噬381±17个酵母细胞，而糖尿病大鼠的中性粒细胞吞噬282±16个酵母细胞，吞噬效率差异显著（p < 0.001）。此外，糖尿病中性粒细胞的吞噬百分比和吞噬效率均与其相应血浆葡萄糖水平呈负相关（分别为p = 0.02；r = -0.498和p < 0.05；r = -0.43），这表明血浆葡萄糖升高会降低中性粒细胞的吞噬能力。对照中性粒细胞未观察到这种关系。这些数据清楚地表明，链脲佐菌素（STZ）诱导的糖尿病大鼠中PMN功能发生改变，高血糖可能是其功能受损导致许多感染性发作的原因。
