Phagocytic and oxidative burst activity of neutrophils in type 2 diabetic patients with foot ulcers
DOI:
https://doi.org/10.51248/.v41i4.1122Keywords:
Neutrophil phagocytic index, respiratory burst, type 2 DM patients, diabetes, foot ulcers, predictors for treatment efficacy of foot ulcersAbstract
Introduction and Aim: Diabetic foot ulcers are common complications seen in diabetic patients. Treatment of this disabling foot sore remains a challenge to health care professionals. This study aimed at evaluating whether the neutrophils from type 2 diabetic patients with foot ulcers present an impairment of phagocytic index and impairment in respiratory burst. We also aimed at understanding whether the impairment in neutrophil phagocytic activity can be alleviated with short course of standard treatment regime for foot ulcers.
Methodology: For this case-controled study, 43 participants with type 2 diabetes (18 with foot ulcers and 25 without foot ulcers) were prospectively recruited along with 18 healthy volunteers. Phagocytic activity of neutrophils and respiratory burst of neutrophils was assessed along with ESR, percentage neutrophil counts before and after 2 weeks of standard treatment for foot ulcers.
Results: Neutrophils of type 2 diabetic patients (with and without foot ulcers ) showed lower levels of phagocytic index and lower percentage of respiratory burst on comparison with non-diabetic subjects. Furthermore, on receiving treatment for foot ulcers, a significant improvement in neutrophil phagocytic indices were observed, along with improvement in wound ulcer score.
Conclusion: Phagocytic activity of the neutrophils is impaired in type 2 diabetics (with and without foot ulcers). Neutrophil phagocytic indices can be improved on glycemic control. Additionally, improvement in neutrophil phagocytic indices after short course treatment for foot ulcers can be useful markers to predict treatment efficacy and in prognosis of diabetic foot ulcers.
References
Brem, H., Tomic-Canic, M. Cellular and molecular basis of wound healing in diabetes. J Clin Invest 2007; 117: 1219-1222.
Gibson, T. B., Driver, V. R., Wrobel, J. S., Christina, J. R., Bagalman, E., DeFrancis, R., et al., Podiatrist care and outcomes for patients with diabetes and foot ulcer. Int Wound J. 2013; 11: 641-648.
Yazdanpanah, L., Shahbazian, H., Nazari, I., Arti, H. R., Ahmadi, F., Mohammadianinejad, S. E., et al., Incidence and risk factors of diabetic foot ulcer: A population-based diabetic foot cohort (ADFC Study)-Two-year follow-up study. Int J Endocrinol. 2018; 2018: 1-9.
Razmpoor, M., Kheirandish, M., Zare, S. Evaluation of predictive factors of development of type 2 diabetes mellitus (T2Dm) in patients with gestational diabetes mellitus. Acta Health Medica. 2017; 2: 229-234.
Giugliano, D., Ceriello, A., Paolisso, G. Oxidative stress and diabetic vascular complications. Diabetes Care. 1996; 19: 257-267.
Lecube, A., Pachon, G., Petriz, J., Hernandez, C., Simo, R. Phagocytic activity is impaired in type 2 diabetes mellitus and increases after metabolic improvement. PLoS One 2011; 6: 1-6.
Markhoffer, W., Stein, M., Maeser, E., Federlin, K. Impairment of polymorphonuclear leukocyte function and metabolic control of diabetes. Diabetes Care 1992; 15: 256-260.
Inoue, S., Lan, Y., Muran, J., Tsuji, M. Reduced hydrogen peroxide production in neutrophils from patients with diabetes. Diabetes Res Clin Pract. 1996; 33: 119-127.
McManus, L. M., Blood, R. C., Prihoda, T. J., Blodgett, J. L., Pinckard, R. N. Agonist-dependent failure of neutrophil function in diabetes correlates with extent of hyperglycemia. J Leukoc Biol. 2001; 70: 395-404.
Bayraktutan, U. Free radicals, diabetes and endothelial dysfunction. Diabetes Obes Metab. 2002; 4: 224-238.
Khondkaryan, L., Margaryan, S., Poghosyan, D., Manukyan, G. Impaired inflammatory response to LPS in type 2 diabetes mellitus. Int J Inflam. 2018; 2018: 1-6.
Forman, H. J. Use and abuse of exogenous H2O2 in studies of signal transduction. Free Radic Biol Med. 2007; 42: 926-932.
Defronzo, R. A., Mandarino, L., Ferrannini, E. Metabolic and molecular pathogenesis of type 2 diabetes mellitus. International Textbook of Diabetes Mellitus. 2003.
Al-Shibly, I. K., Alhamdany, M. H., Al-Kaif, R. A. I., Al-Kaif, L. A. immunological base behind the increased susceptibility of diabetic patients for infections. Indian J Public Health Res Dev. 2019; 10: 3047-3051.
Muniz-Junqueira, M. I., Pecanha, L. M. F., Silva-Filho, V. L., Almeida Cardoso, M. C., Tosta, C. E. Novel microtechnique for assessment of post-natal maturation of phagocytic functions of neutrophils and monocytes. Clin Diagn Lab Immunol 2003; 10: 1096-1102.
Campbell, D. E., Douglas, S. D. Phagocytic cell functions. I. Oxidation and chemotaxis. In: Rose NR, de Macario EC, Folds JD, Lane HC, Nakamura RM (eds) Manual of Clinical Laboratory Immunology, 5th edition American Society for Microbiology, Washington. 1997; 320-328.
Larijani, B., Shooshtarizadeh, P., Mosaffa, N., Heshmat, R. Polymorphonuclear leucocyte respiratory burst activity correlates with serum zinc level in type 2 diabetic patients with foot ulcers. Br J Biomed Sci 2007; 64: 13-17.
Top, C., Yildiz, S., Öncül, O., Qydedi, T., Cevikbas, A., Soyogul, U.G., et al., Phagocytic activity of neutrophils improves over the course of therapy of diabetic foot infections. J Infect. 2007; 55: 369-373.
Santema, T. B. K., Poyck, P. P. C., Ubbink, D. T. Systematic review and meta-analysis of skin substitutes in the treatment of diabetic foot ulcers: Highlights of a Cochrane systematic review. Wound Repair Regen. 2016; 24: 737-744.
Fovenyi, J., Totpal, K., Thaisz, E., Garam, T. Non-specific cellular immunity in type I and type II diabetes. Exp Clin Endocrinol. 1984; 83: 203-206.
Inoguchi, T., Sonata, T., Tsubouchi, H., Etoh, T., Kakimoto, M., Sonoda, N., et al., Protein kinase c-dependent increase in reactive oxygen species (ROS) Production in Vascular Tissues of diabetes: role of vascular NAD(P)H oxidase. J Am Soc Nephrol. 2003; 14: S227-S232.
Prompers, L., Huijberts, M., Apelqvist, J., Jude, E., Piaggesi, A., Edmonds, M., et al., High prevalence of ischaemia, infection and serious comorbidity in patients with diabetic foot disease in Europe. Baseline results from the Eurodiale study. Diabetologia. 2007; 50: 18-25.
Karahan, S. C., De?er, O., Örem, A., Ucar, F., Erem, C., Alver, A., et al., The effects of impaired trace element status on polymorphonuclear leukocyte activation in the development of vascular complications in type 2 diabetes mellitus. Clin Chem Lab Med. 2001; 39: 109-115.
Kaul, C., Ramarao, P. The role of aldose reductase inhibitors in diabetic complications: Recent trends. Methods Find Exp Clin Pharmacol. 2001; 23: 465-475.
Patti, M. E., Corvera, S. The role of mitochondria in the pathogenesis of type 2 diabetes. Endocr. Rev 2010; 31: 364-395.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2021 Biomedicine
This work is licensed under a Creative Commons Attribution 4.0 International License.
Plum Analytics