NOD1 receptor is up-regulated in diabetic human and murine myocardium

2014 ◽  
Vol 127 (12) ◽  
pp. 665-677 ◽  
Author(s):  
Patricia Prieto ◽  
María Teresa Vallejo-Cremades ◽  
Gemma Benito ◽  
Pilar González-Peramato ◽  
Daniel Francés ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Immune System ◽  
Innate Immune System ◽  
Innate Immune ◽  
Murine Models

We demonstrate that the myocardium from murine models of diabetes and the myocardium of patients with Type 2 diabetes overexpress the receptor of the innate immune system NOD1. This up-regulation occurred in cardiomyocytes and was associated with an increased apoptotic profile.

scholarly journals Vitamin D and inflammation in the prevention of type 2 diabetes: public health relevance

2012 ◽  
Vol 3 (4) ◽  
pp. 243
Author(s):  
Alaa Badawi ◽  
Eman Sadoun ◽  
Mohamed H. Al Thani
Keyword(s):  
Public Health ◽  
Type 2 Diabetes ◽  
Vitamin D ◽  
Immune System ◽  
Innate Immune System ◽  
Population Level ◽  
Innate Immune ◽  
Low Grade ◽  
Low Grade Inflammation

The incidence of type 2 diabetes mellitus (T2DM) is increasing worldwide. To reduce the disease risk and burden at the population level, preventative strategies should be developed with minimal cost and effort and with no side-effects. Low-grade inflammation resulting from imbalances in the innate immune system has been associated with an array of chronic disorders that predispose to the later development of T2DM (e.g., obesity, metabolic syndrome, and insulin resistance). As a result, inflammation may contribute to the pathogenesis of T2DM. Therefore, attenuation of this inflammatory response via modulating the innate immune system could lead to improved insulin sensitivity and delayed disease onset. Dietary supplementation with vitamin D may represent a novel strategy toward the prevention and control of T2DM at the population level due to its anti-inflammatory and antioxidant properties. This review examines current knowledge linking T2DM to chronic low-grade inflammation and the role of vitamin D in modulating this relationship. The concept that vitamin D, via attenuating inflammation, could be employed as a novel preventive measure for T2DM is evaluated in the context of its relevance to health care and public health practices.

scholarly journals Is Type 2 Diabetes an Autoimmune-Inflammatory Disorder of the Innate Immune System?

Endocrinology ◽  
2005 ◽  
Vol 146 (10) ◽  
pp. 4189-4191 ◽  
Author(s):  
Leonard D. Kohn ◽  
Brian Wallace ◽  
Frank Schwartz ◽  
Kelly McCall
Keyword(s):  
Type 2 Diabetes ◽  
Immune System ◽  
Innate Immune System ◽  
Innate Immune ◽  
Inflammatory Disorder

scholarly journals Vitamin D and inflammation in the prevention of type 2 diabetes: public health relevance

2012 ◽  
Vol 3 (4) ◽  
pp. 243-255 ◽  
Author(s):  
Alaa Badawi ◽  
Eman Sadoun ◽  
Mohamed H. Al Thani
Keyword(s):  
Public Health ◽  
Type 2 Diabetes ◽  
Vitamin D ◽  
Immune System ◽  
Innate Immune System ◽  
Population Level ◽  
Innate Immune ◽  
Low Grade ◽  
Low Grade Inflammation

The incidence of type 2 diabetes mellitus (T2DM) is increasing worldwide. To reduce the disease risk and burden at the population level, preventative strategies should be developed with minimal cost and effort and with no side-effects. Low-grade inflammation resulting from imbalances in the innate immune system has been associated with an array of chronic disorders that predispose to the later development of T2DM (e.g., obesity, metabolic syndrome, and insulin resistance). As a result, inflammation may contribute to the pathogenesis of T2DM. Therefore, attenuation of this inflammatory response via modulating the innate immune system could lead to improved insulin sensitivity and delayed disease onset. Dietary supplementation with vitamin D may represent a novel strategy toward the prevention and control of T2DM at the population level due to its anti-inflammatory and antioxidant properties. This review examines current knowledge linking T2DM to chronic low-grade inflammation and the role of vitamin D in modulating this relationship. The concept that vitamin D, via attenuating inflammation, could be employed as a novel preventive measure for T2DM is evaluated in the context of its relevance to health care and public health practices.

scholarly journals Type 2 Diabetes, PUFAs, and Vitamin D: Their Relation to Inflammation

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Ana L. Guadarrama-López ◽  
Roxana Valdés-Ramos ◽  
Beatríz E. Martínez-Carrillo
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Vitamin D ◽  
Innate Immune System ◽  
Inflammatory Diseases ◽  
Innate Immune ◽  
Important Public Health ◽  
Chronic Inflammatory Diseases ◽  
Treatment And Prevention

Chronic diseases have become one of the most important public health problems, due to their high costs for treatment and prevention. Until now, researchers have considered that the etiology of Type 2 diabetes mellitus (T2DM) is multifactorial. Recently, the study of the innate immune system has offered an explanation model of the pathogenesis of T2DM. On the other hand, there is evidence about the beneficial effect of polyunsaturated fatty acids (PUFA) n-3 and n-6 in patients with chronic inflammatory diseases including diabetes. Furthermore, high vitamin D plasmatic concentrations have been associated with the best performance of pancreaticβcells and the improving of this disease. In conclusion, certain fatty acids in the adequate proportion as well as 25-hydroxivitamin D can modulate the inflammatory response in diabetic people, modifying the evolution of this disease.

Abstract 551: Loss of ABCG1 Specifically in Pulmonary Type 2 Cells Results in Impaired Surfactant Lipid Metabolism

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Thomas Q de Aguiar Vallim ◽  
David J Merriott ◽  
Joan Cheng ◽  
Angela Cheng ◽  
Angel Baldan ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Immune System ◽  
B Cells ◽  
Innate Immune System ◽  
The United States ◽  
Natural Antibodies ◽  
Innate Immune ◽  
Whole Body ◽  
Lamellar Bodies

Cardiovascular disease (CVD) is the leading cause of death in the United States, and patients with pulmonary disease are at least 2-fold more likely to develop cardiovascular complications. Whole-body cholesterol balance is a complex and tightly regulated process. The sterol-transporter ATP Binding Cassette transporter G1 (ABCG1) is critical for maintaining normal cellular cholesterol and lipid homeostasis. After the liver and intestine, the lung is the 3rd most active lipid-secreting organ. Pulmonary alveolar proteinosis (PAP) is a rare lung disease characterized by the accumulation of surfactant lipids and proteins in the pulmonary alveoli resulting in respiratory distress. For almost all reported cases the underlying cause is unknown. Synthesis and secretion of surfactant in the lung is restricted to epithelial type 2 pneumocytes (T2 cells). However, subsequent clearance of surfactant from the hypophase is dependent upon both T2 cells and macrophages. Both T2 cells and macrophages express high levels of ABCG1. Abcg1-/- mice develop a severe pulmonary lipidosis, characterized by elevated levels of multiple lipid species and the presence of lipid-loaded macrophages and T2 cells containing abnormal lamellar bodies. Recent advances have also implicated a role for the innate immune system in the pathogenesis of PAP. We recently demonstrated that the lungs of Abcg1-/- mice exhibit a profound immune response associated with a local increase in innate immune natural antibody-secreting B-1 B cells and both local and circulating natural antibodies. Here we show that mice lacking ABCG1 specifically in T2 cells develop abnormal lamellar bodies with altered phospholipid and cholesterol homeostasis, and altered gene expression. Collectively, our results suggest that ABCG1 is critical for normal surfactant metabolism and that the pulmonary expansion of B-1 B cells and the subsequent increase in natural antibodies in Abcg1-/- mice may provide a novel model in which to study the role of the innate immune system in PAP, and the subsequent risk of developing cardiovascular disease.

The innate immune system and diabetes mellitus: the relevance of periodontitis? A hypothesis

2010 ◽  
Vol 119 (10) ◽  
pp. 423-429 ◽  
Author(s):  
Martin G. Lazenby ◽  
Martin A. Crook
Keyword(s):  
Diabetes Mellitus ◽  
Immune System ◽  
Fetal Programming ◽  
Innate Immune System ◽  
Inflammatory Process ◽  
Innate Immune ◽  
Acute Phase Reactants ◽  
The Metabolic Syndrome ◽  
Type 2 Dm

About a decade ago, a hypothesis was proposed suggesting that the innate immune system, including acute-phase reactants, contribute to the development of T2DM [Type 2 DM (diabetes mellitus)] and the metabolic syndrome. In this model, it was hypothesized that the innate immune system modulates the effects of many factors, including genes, fetal programming, nutrition and aging, upon the later development of metabolic problems associated with insulin resistance. In this present article, we expand this hypothesis by looking at the involvement of periodontitis in DM and its complications. Periodontitis is a common inflammatory process involving the innate immune system and is associated with DM. We will also illustrate how dental disease is important in patients with DM and could be implicated in various diabetic complications.

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