Dynamics of Inflammatory Mediators in Patients with the Neuroischemic Form of Diabetic Foot Syndrome | Ukrainian Medical Journal

Inflammation is an adaptive response of the body to injury, involving vascular-mesenchymal changes and the interaction of mediators. Cytokines play a key role in the inflammatory response by regulating immune cell activation and the production of pro-inflammatory and anti-inflammatory factors. Inflammation in diabetic foot syndrome has significant clinical relevance and may lead to severe complications. Wound healing occurs in four phases, during which macrophages, fibroblasts, and growth factors coordinate tissue repair. Nitric oxide is involved in inflammation regulation, and its deficiency contributes to vascular dysfunction. Oxidative stress and uncontrolled cytokine production may hinder the healing process and impair microcirculation.

Object and methods of study. The study was conducted at the Department of Purulent Surgery of the Municipal Non-Profit Enterprise «Kyiv City Clinical Hospital № 6» in 2023. A total of 115 patients with diabetic foot syndrome were treated, of whom 35 patients with the neuroischemic form of diabetic foot syndrome were included in the study. The study focused on the dynamics of inflammatory mediators in these patients.

Results. The conducted research demonstrated the dynamics of inflammatory mediators in patients with the neuroischemic form of diabetic foot syndrome.

References

1. Струков А.І., Сєров В.В. (2004) Патологічна анатомія (вид. 4). Факт, Харків, 864 с.
2. Біляєва О.О., Козинець Г.П., Осадча О.І. та ін. (2019). Роль оксиду азоту в розвитку ендотеліальних дисфункцій при синдромі діабетичної стопи. doi.org/10.34287/MMT.4(43).2019.5.
3. Singer A.J., Clark R.A. (1999) Cutaneous wound healing. N. Engl. J. Med., 341: 738–746.
4. Kane C.J., Hebda P.A., Mansbridge J.N., Hanawalt P.C. (1991) Direct evidence for spatial and temporal regulation of transforming growth factor beta 1 expression during cutaneous wound healing. J. Cell. Physiol., 148(1): 157–173.
5. Igarashi A., Okochi H., Bradham D.M., Grotendorst G.R. (1993) Regulation of connective tissue growth factor gene expression in human skin fibroblasts and during wound repair. Mol. Biol. Cell, 4(6): 637–645.
6. Marchese C., Felici A., Visco V. et al. (2001) Fibroblast growth factor 10 induces proliferation and differentiation of human primary cultured keratinocytes. J. Invest. Dermatol., 116(4): 623–628.
7. Werner S., Beer H.D., Mauch C. et al. (2001) The Mad1 transcription factor is a novel target of activin and TGF-beta action in keratinocytes: possible role of Mad1 in wound repair and psoriasis. Oncogene, 20(51): 7494–7504.
8. Kawana S. (1996) The membrane attack complex of complement alters the membrane integrity of cultured endothelial cells:a possible patophisiology for immune complex vasculitis. Acta Dermato-Venerologica, 76(1): 13–21.
9. Bachschmid M., Thurau S., Zou M.H., Ullrich V. (2003) Endothelial cell activation by endotoxin involves superoxide/NO-mediated nitration of prostacyclin syn- thase and tromboxane receptor stimulation. FASEB J., 17: 914–916.
10. Ahsa H., AH A., Ali R. (2003) Oxygen free radicals and systemic autoimmunity. Clin. Exp. Immunol., 131(3): 398–404.
11. Forstermann U. (2006) Endotelial NO synthase as a source of NO and superoxide. Eur. J. Clin. Pharmacol., 62(Supll. 13): 5–12.
12. Jourd’heuil D., Hallén K., Feelisch M., Grisham M.B. (2000) Dynamic state of S-nitrosothiols in human plasma and whole blood. Free Radic. Biol. Med., 28(3): 409–417. doi: 10.1016/s0891-5849(99)00257-9.
13. Moshage H., Kok B., Huizenga J.R., Jansen P.L. (1995) Nitrite and nitrate determinations in plasma: a critical evaluation. Clin. Chem., 41(6 Pt. 1): 892–896.
14. Zhao R., Liang H., Clark E. et al. (2016) Inflammation in chronic wounds. Intl. J. Mol. scientific, 17: 2085.
15. Nguyen T.T., Dean D., Walter W.R. et al. (2018) Validation of matrix metalloproteinase-9 (MMP-9) as a novel target for the treatment of diabetic foot ulcers in humans and discovery of a potent and selective small molecule inhibitor of MMP-9 that accelerates healing. J. Med. Chem., 61: 8825–8837.
16. Julier Z., Park A.J., Briques P.S., Martino M.M. (2017) Promoting tissue regeneration by modulating the immune system. Acta Biomater., 53: 13–28.
17. Razieva K., Kim Y., Zharkinbekov Z. et al. (2021) Immunology of acute and chronic wound healing. Biomolecules, 11: 700.
18. Kono K., Koya-Miyata S., Harashima A. et al. (2021) Inflammatory M1-like NK-4-polarized macrophages undergo an enhanced phenotypic switch to an anti-inflammatory M2-like phenotype when cocultured with apoptotic cells. J. Inflamm., 18: 2.
19. Xu Z., Liang B., Tian J., Wu J. (2021) Anti-inflammatory biomaterial platforms for chronic wound healing. Biomater. Sci., 9: 4388–4409.
20. Champeau M., Povoa V., Militao L. et al. (2018) Supramolecular poly(acrylic acid)/hydrogel F127 with hydration-controlled nitric oxide release to improve wound healing. Acta Biomater., 74: 312–325.
21. Dunnill K., Patton T., Brennan J. et al. (2017) Reactive oxygen species (ROS) and wound healing: functional role of ROS and new technologies that modulate ROS to accelerate the healing process. Intl. Wounded J., 14: 89–96.
22. Hong W.X., Hu M.S., Esquivel M. et al. (2014) The role of hypoxia-inducible factor in wound healing. Add. Wound Care, 3: 390–399.
23. Brauweiler A.M., Goleva E., Hall K.F., Leung D.Yu. (2015) Th2 cytokines suppress lipoteichoic acid-induced matrix metalloproteinase expression and keratinocyte migration in response to wounding. Jay Invest. Dermatol., 135: 2550–2553.
24. Leoni G., Neumann P.A., Sumagin R. et al. (2015) Wound repair: the role of immuno-epithelial interactions. Mucosal. Immunol., 8: 959–968.