scholarly journals Leukocyte Adhesion Molecules in Diabetic Retinopathy

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Kousuke Noda ◽  
Shintaro Nakao ◽  
Susumu Ishida ◽  
Tatsuro Ishibashi
Keyword(s):  
Diabetic Retinopathy ◽  
Adhesion Molecules ◽  
Leukocyte Adhesion ◽  
Microvascular Complications ◽  
Systemic Disease ◽  
Low Grade ◽  
Adhesion Molecule Expression ◽  
Adhesive Interactions ◽  
Low Grade Inflammation ◽  
Leukocyte Adhesion Molecules

Diabetes is a systemic disease that causes a number of metabolic and physiologic abnormalities. One of the major microvascular complications of diabetes is diabetic retinopathy (DR), a leading cause of blindness in people over age 50. The mechanisms underlying the development of DR are not fully understood; however, extensive studies have recently implicated chronic, low-grade inflammation in the pathophysiology of DR. During inflammation leukocytes undergo sequential adhesive interactions with endothelial cells to migrate into the inflamed tissues, a process known as the “leukocyte recruitment cascade” which is orchestrated by precise adhesion molecule expression on the cell surface of leukocytes and the endothelium. This paper summarizes the recent clinical and preclinical works on the roles of leukocyte adhesion molecules in DR.

Molecular and Pathophysiological Mechanisms of Diabetic Retinopathy in Relation to Adhesion Molecules

2019 ◽  
Vol 15 (5) ◽  
pp. 363-371 ◽  
Author(s):  
Salini Scaria Joy ◽  
Khalid Siddiqui
Keyword(s):  
Diabetic Retinopathy ◽  
Endothelial Cell ◽  
Endothelial Function ◽  
Adhesion Molecules ◽  
Inflammatory Factors ◽  
Low Grade ◽  
Pathophysiological Mechanisms ◽  
Low Grade Inflammation ◽  
Slow Rolling

Diabetic Retinopathy (DR) is considered as a most common microvascular complication of diabetes affected by one in three people who are suffered for diabetes. Several pathophysiological mechanisms and adhesion molecules may play an etiologic role in the development of diabetes and its complications. The adhesion molecules located on both leucocytes and endothelial cells and considered as important molecules which can assessed the endothelial function. The functions of adhesion molecules involved in the cellular margination, slow rolling and transmigration of leukocytes. Hyperglycemia and its immediate biochemical sequelae or the low-grade inflammation directly alter endothelial function or influence endothelial cell functioning indirectly by induce oxidative stress and activates leukocytosis and leukocyte-endothelial cell interactions by the increased expression of adhesion molecules, growth factors, inflammatory factors, chemokines etc. and results DR. This review summarized the several pathophysiological mechanisms and role of adhesion molecules in disruption of homeostasis of vasculature by leukocytes in the development of diabetic retinopathy.

scholarly journals Induction of leukocyte adhesion molecules and renal physiologically active molecules in Porphyromonas gingivalis lipopolysaccharide-induced diabetic nephropathy

2020 ◽  
Author(s):  
Koichiro Kajiwara ◽  
Yoshihiko Sawa ◽  
Takahiro Fujita ◽  
Sachio Tamaoki
Keyword(s):  
Diabetic Nephropathy ◽  
Adhesion Molecules ◽  
Leukocyte Adhesion ◽  
Diabetic Mouse ◽  
Renal Parenchyma ◽  
Periodontal Pathogen ◽  
Diabetic Patients ◽  
Renal Tubules ◽  
Diabetic Mice ◽  
Leukocyte Adhesion Molecules

Abstract Background We recently reported that the glomerular endothelium expresses toll-like receptor (TLR)2 and TLR4 in diabetic environments and established that the TLR2 ligand Porphyromonas (P.) gingivalis lipopolysaccharides (LPS) induces nephropathy in diabetic mice. It is thought that P. gingivalis LPS promotes the chronic inflammation with the overexpression of leukocyte adhesion molecules and renal-specific metabolic enzymes by the recognition of P. gingivalis LPS via TLR in the diabetic kidneys. The present study aims to examine the expression of leukocyte adhesion molecules and renal metabolic factors in mouse kidneys with periodontal pathogen P. gingivalis LPS-induced diabetic nephropathy that was recently established. Methods The immunohistochemical investigation was performed on mouse kidney with P. gingivalis LPS-induced diabetic nephropathy model with glomerulosclerosis in glomeruli. Results There were no vessels which expressed vascular cell adhesion molecule-1 (VCAM-1), E-selectin, or fibroblast growth factor (FGF) 23 in diabetic mice, or in healthy mice administered P. gingivalis LPS. However, in diabetic mouse kidneys with P. gingivalis LPS-induced nephropathy the expression of VCAM-1 and the accumulation of FGF23 were established in renal tubules and glomeruli, and the expression of E-selectin was established in renal parenchyma and glomeruli. The angiotensin-converting enzyme 2 (ACE2) was detected in the proximal tubules but not in other regions including not in distal tubules of diabetic mice without LPS, and not in healthy mice administered P. gingivalis LPS. In diabetic mouse kidneys with P. gingivalis LPS-induced nephropathy ACE2 was detected both in renal tubules as well as in glomeruli. The macrophage-1 (Mac-1) and podoplanin-positive cells increased in the renal parenchyma with diabetic condition and there was accumulation in P. gingivalis LPS-induced diabetic nephropathy. As the expression of VCAM-1 and E-selectin is upregulated in glomeruli, tubules, and intertubular capillaries, it is thought that the inflammatory infiltration of the monocyte-macrophage lineage promoted in kidneys with P. gingivalis LPS-induced the diabetic nephropathy. Conclusions P. gingivalis LPS may progressively accelerate the development of the renal inflammatory environment in LPS-accumulated glomeruli with the macrophage infiltration via the renal expression of VCAM-1 and E-selectin, and with ACE2 overexpression and FGF23 accumulation. Periodontitis may be a critical factor in the progress of nephropathy in diabetic patients.

scholarly journals NAFLD and Infection, a Nuanced Relationship

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Abimbola Adenote ◽  
Igor Dumic ◽  
Cristian Madrid ◽  
Christopher Barusya ◽  
Charles W. Nordstrom ◽  
...  
Keyword(s):  
Current Knowledge ◽  
Systemic Disease ◽  
Type Ii Diabetes Mellitus ◽  
Low Grade ◽  
Extrahepatic Manifestations ◽  
Nonalcoholic Fatty Liver ◽  
Multiple Organs ◽  
Clostridioides Difficile ◽  
Low Grade Inflammation ◽  
Ovarian Syndrome

The prevalence of nonalcoholic fatty liver disease (NAFLD) has increased significantly over the last few decades mirroring the increase in obesity and type II diabetes mellitus. NAFLD has become one of the most common indications for liver transplantation. The deleterious effects of NAFLD are not isolated to the liver only, for it has been recognized as a systemic disease affecting multiple organs through protracted low-grade inflammation mediated by the metabolic activity of excessive fat tissue. Extrahepatic manifestations of NAFLD such as cardiovascular disease, polycystic ovarian syndrome, chronic kidney disease, and hypothyroidism have been well described in the literature. In recent years, it has become evident that patients suffering from NAFLD might be at higher risk of developing various infections. The proposed mechanism for this association includes links through hyperglycemia, insulin resistance, alterations in innate immunity, obesity, and vitamin D deficiency. Additionally, a risk independent of these factors mediated by alterations in gut microbiota might contribute to a higher burden of infections in these individuals. In this narrative review, we synthetize current knowledge on several infections including urinary tract infection, pneumonia, Helicobacter pylori, coronavirus disease 2019, and Clostridioides difficile as they relate to NAFLD. Additionally, we explore NAFLD’s association with hidradenitis suppurativa.

Proliferation of resting lymphocytes is induced by triggering T cells through an epitope common to the three CD18/CD11 leukocyte adhesion molecules

1991 ◽  
Vol 136 (2) ◽  
pp. 519-524 ◽  
Author(s):  
Violaine David ◽  
Gerald Leca ◽  
Nathalie Corvaia ◽  
Francoise le Deist ◽  
Laurence Boumsell ◽  
...  
Keyword(s):  
T Cells ◽  
Adhesion Molecules ◽  
Leukocyte Adhesion ◽  
Resting Lymphocytes ◽  
Leukocyte Adhesion Molecules

Leukocyte adhesion molecules as a cofactor in AIDS: Basic science and pilot study

1995 ◽  
Vol 45 (2) ◽  
pp. 164-168 ◽  
Author(s):  
A.D. Allen ◽  
D.N. Hart ◽  
M.K. Hechinger ◽  
M.J. Slattery ◽  
C.V. Chesson ◽  
...  
Keyword(s):  
Pilot Study ◽  
Adhesion Molecules ◽  
Basic Science ◽  
Leukocyte Adhesion ◽  
Leukocyte Adhesion Molecules
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