Type 2 Diabetes Mellitus Provokes Rat Immune Cells Recruitment into the Pulmonary Niche by Up-regulation of Endothelial Adhesion Molecules

Purpose: Diabetes mellitus, especially type 2, is conceived as a devastating chronic metabolicdisease globally. Due to the existence of an extensive vascular network in the pulmonary tissue,it is suggested that lungs are sensitive to the diabetic condition like other tissues. This studywas designed to address the possible effect of type 2 diabetes mellitus on the promotion ofpathological changes via vascular injury.Methods: Sixteen male Wistar rats were randomly allocated to the two of control and T2D groups.To induce type 2 diabetes (T2D), rats were received high-fat and a single dose of streptozotocin(STZ). On week 12, rats were euthanized and lungs samples were taken. Using hematoxylin andeosin (H&E) staining, the pathological changes were monitored. The expression of intercellularadhesion molecule (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and interleukin10 (IL-10) was monitored using real-time PCR assay. The level of tumor necrosis factor-α (TNF-α)was detected using ELISA assay. Nitrosative stress was monitored using the Griess assay.Results: Pathological examination in bronchoalveolar discharge revealed the existence of mildto moderate interstitial bronchopneumonia and increased neutrophilic leukocytosis comparedto the control. Enhanced ICAM-1 and VCAM-1 expression and suppression of IL-10 was foundusing real-time PCR analysis (P < 0.05). The levels of TNF-α and NO were increased withdiabetic changes compared to the control rats (P < 0.05).Conclusion: T2D could promote pulmonary tissue injury via the production of TNF-α and upregulationof vascular ICAM-1 and VCAM-1. The inflammatory status and vascular ICAM-1 andVCAM-1 increase immune cell recruitment into the pulmonary niche.