title: Polymorphonuclear neutrophil dysfunctions in streptozotocin-induced type 1 diabetic rats.
abstract: 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.
authors.affiliation: Department of Biochemistry and Molecular Biology, University of Dhaka, Dhaka-1000, Bangladesh. nurunnabi369@yahoo.com
authors.forename: A H M Nurun
authors.initials: AH
authors.lastname: Nabi
authors.forename: Laila N
authors.initials: LN
authors.lastname: Islam
authors.forename: Mohammad Mahfuzur
authors.initials: MM
authors.lastname: Rahman
authors.forename: Kazal Boron
authors.initials: KB
authors.lastname: Biswas
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000097:blood*; D003922:Diabetes Mellitus, Type 1 / Q000097:blood*; D005260:Female; D005947:Glucose / Q000378:metabolism; D007960:Leukocyte Disorders / Q000150:complications / Q000209:etiology; D008297:Male; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000378:metabolism* / Q000473:pathology*; D010587:Phagocytosis; D051381:Rats; D020318:Rats, Long-Evans; D012441:Saccharomyces cerevisiae / Q000378:metabolism; D013311:Streptozocin / Q000494:pharmacology
chemical_list: D009240:N-Formylmethionine Leucyl-Phenylalanine; D013311:Streptozocin; D005947:Glucose