**2. Inflammation and diabetic retinopathy**

Inflammation is defined as the body's mechanism of self-defense against pathogens. In this complex process, mediators such as pro-inflammatory cytokines, chemokines and adhesion molecules are involved. They initiate the interaction between the endothelium and leukocytes and consequently induce the migration of leukocytes towards the injured or infected tissue [5]. Although acute inflammation is considered beneficial, a chronic and dysregulated one produces harmful effects, being known to be involved in diseases such as rheumatoid arthritis, multiple sclerosis and atherosclerosis [5].

Lutty et al. were the first who reported an increased neutrophil number per square millimeter in both retinal and choroidal vessels in DR patients [6]. Moreover, they continued the study of neutrophils in diabetic monkeys and found an association between the accumulation of neutrophils and capillary closure [7]. Further studies found evidence that capillary occlusion and intraretinal neovascularization are associated with the attachment of neutrophils and monocytes [8], while the level of leukocytes adherence to the retinal vasculature, known as leukostasis, is associated with the progression of DR [9]. Recent findings implicate that an increase of ICAM-1 and integrins at the level of endothelial cells and leukocytes is responsible for the increase in leukostasis, while ICAM-1 blocking and CD18 deletion decreases the leukostasis induced by DM [10, 11]. Microglial cell is a resident macrophage distributed throughout the retina, which releases inflammatory cytokines such as TNF-α after being activated [12].

There are several processes in DR pathogenesis in which inflammation is involved:


*Local Inflammatory Biomarkers and Potential Inflammation-Targeting Therapies in Diabetic… DOI: http://dx.doi.org/10.5772/intechopen.99807*

DM causes increased systemic and local production of numerous inflammatory molecules involved in DR onset and development.
