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

Abstract

Purpose: Diabetes mellitus, especially type 2, is conceived as a devastating chronic metabolic disease 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 study was designed to address the possible effect of type 2 diabetes mellitus on the promotion of pathological 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, rats were received high-fat and a single dose of STZ. On week 12, rats were euthanized and lungs samples were taken. Using Hematoxylin and Eosin staining, the pathological changes were monitored. The expression of vascular ICAM-1 and VCAM-1, and IL-10 was monitored using real-time PCR assay. The level of 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 mild to moderate interstitial bronchopneumonia and increased neutrophilic leukocytosis compared to the control. Enhanced ICAM-1 and VCAM-1 expression and suppression of IL-10 was found using real-time PCR analysis (p<0.05). The levels of TNF-α and NO were increased with diabetic changes compared to the control rats (p<0.05). Conclusion T2D could promote pulmonary tissue injury via the production of TNF-α and up-regulation of vascular ICAM-1 and VCAM-1. The inflammatory status and vascular ICAM-1 and VCAM-1 increase immune cell recruitment into the pulmonary niche.

Type 2 diabetes mellitus stimulated pulmonary vascular inflammation and exosome biogenesis in rats

“…They concluded that increased Exo can be associated with inflammatory responses. More recently, our team found that the inflammatory responses were increased after immune cell recruitment into the lung tissues in a rat model of T2DM 41 . A growing body of evidence indicates that T2DM is associated with hypoxia, proinflammation, oxidative stress, and immune cell infiltration, which may modulate Exo biogenesis in several cell types 42,43 .…”

“…More recently, our team found that the inflammatory responses were increased after immune cell recruitment into the lung tissues in a rat model of T2DM. 41 A growing body of evidence indicates that T2DM is associated with hypoxia, proinflammation, oxidative stress, and immune cell infiltration, which may modulate Exo biogenesis in several cell types. 42,43 It seems that the promotion of vascular inflammation can stimulate subsequent immune cell recruitment into the lung parenchyma, leading to immune cell chemotaxis and secretion of inflammatory cytokines under pathological conditions.…”

Type 2 diabetes and its effects on microRNA-155 and microRNA-133a expression in lung tissue of male rats

“…T2D was acclimatized by a HFD (22% fat, 20% protein, and 48% carbohydrate) for four weeks, followed by intraperitoneal injection of a single dose of STZ (35 mg/kg body weight) [27]. To dissolve streptozotocin (STZ), 0.1 M cold citrate buffer with a pH = 4.5 was used.…”

Melatonin reduces lung injury in type 1 diabetic mice by the modulation of autophagy

“…However, the precise mechanism of lung parenchymal damage in diabetes is still not fully understood. Undoubtedly, understanding the precise process of this damage can help manage and lessen the pulmonary difficulties that diabetic individuals experience [ 4 , 5 ]. The lung parenchyma is vulnerable to injury in diabetics due to the high levels of elastin and collagen tissue, as well as the abundance of arterial beds in the lung tissue, on the one hand, and the presence of chronic oxidative stress and systemic inflammation in diabetes, on the other hand [ 6 , 7 ].…”