scholarly journals Effect of vitamin A deficiency on the immune response in obesity

2012 ◽  
Vol 71 (2) ◽  
pp. 290-297 ◽  
Author(s):  
Olga P. García
Keyword(s):  
Vitamin A ◽  
Inflammatory Response ◽  
Chronic Inflammation ◽  
Vitamin A Deficiency ◽  
Critical Role ◽  
Fat Deposition ◽  
Cell Mediated Immunity ◽  
Low Grade ◽  
Th1 Response ◽  
Lower Vitamin

Obesity has been associated with low-grade systemic inflammation and with micronutrient deficiencies. Obese individuals have been found to have lower vitamin A levels and lower vitamin A intake compared with normal-weight individuals. Vitamin A plays a major role in the immune function, including innate immunity, cell-mediated immunity and humoral antibody immunity. It has also been recognised recently that vitamin A has important regulatory functions. Vitamin A status has an important effect on the chronic inflammatory response. Vitamin A deficiency increases a T-helper type 1 (Th1) response, elevates levels of pro-inflammatory cytokines, increases the expression of leptin, resistin and uncoupling proteins (UCP) and promotes adipogenesis. The effect of vitamin A deficiency on obesity might be increasing the risk of fat deposition and also the risk of chronic inflammation associated with obesity. Supplementation with vitamin A in vitro and in animal models has been found to reduce concentrations of adipocytokines, such as leptin and resistin. In conclusion, vitamin A deficiency increases a Th1 response in the presence of obesity and thus, increases the inflammatory process involved in chronic inflammation and fat deposition. The metabolism of leptin and other adipocytokines may play a critical role in the effect of vitamin A deficiency in the inflammatory response observed in obesity.

scholarly journals RNA-binding proteins La and HuR cooperatively modulate translation repression of PDCD4 mRNA

2020 ◽  
pp. jbc.RA120.014894
Author(s):  
Ravi Kumar ◽  
Dipak Kumar Poria ◽  
Partho Sarothi Ray
Keyword(s):  
Inflammatory Response ◽  
Chronic Inflammation ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Critical Role ◽  
Regulation Of Gene Expression ◽  
Mrna Translation ◽  
Suppressor Gene ◽  
Cooperative Action ◽  
Translation Repression

Post-transcriptional regulation of gene expression plays a critical role in controlling the inflammatory response. An uncontrolled inflammatory response results in chronic inflammation, often leading to tumorigenesis. Programmed cell death 4 (PDCD4) is a pro-inflammatory tumor-suppressor gene which helps to prevent the transition from chronic inflammation to cancer. PDCD4 mRNA translation is regulated by an interplay between the oncogenic microRNA miR-21 and the RNA-binding protein (RBP) HuR in response to LPS stimulation, but the role of other regulatory factors remain unknown. Here we report that the RBP Lupus antigen (La) interacts with the 3’UTR of PDCD4 mRNA and prevents miR-21-mediated translation repression. While LPS causes nuclear-cytoplasmic translocation of HuR, it enhances cellular La expression. Remarkably, La and HuR were found to bind cooperatively to the PDCD4 mRNA and mitigate miR-21-mediated translation repression. The cooperative action of La and HuR reduced cell proliferation and enhanced apoptosis, reversing the pro-oncogenic function of miR-21. Together, these observations demonstrate a cooperative interplay between two RBPs, triggered differentially by the same stimulus, which exerts a synergistic effect on PDCD4 expression and thereby helps maintain a balance between inflammation and tumorigenesis.

scholarly journals Nutritional approaches for managing obesity-associated metabolic diseases

2017 ◽  
Vol 233 (3) ◽  
pp. R145-R171 ◽  
Author(s):  
Rachel Botchlett ◽  
Shih-Lung Woo ◽  
Mengyang Liu ◽  
Ya Pei ◽  
Xin Guo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Metabolic Pathways ◽  
Metabolic Diseases ◽  
Critical Role ◽  
Fat Deposition ◽  
Low Grade ◽  
Metabolic Homeostasis ◽  
Peripheral Tissues ◽  
Metabolic Dysregulation

Obesity is an ongoing pandemic and serves as a causal factor of a wide spectrum of metabolic diseases including diabetes, fatty liver disease, and cardiovascular disease. Much evidence has demonstrated that nutrient overload/overnutrition initiates or exacerbates inflammatory responses in tissues/organs involved in the regulation of systemic metabolic homeostasis. This obesity-associated inflammation is usually at a low-grade and viewed as metabolic inflammation. When it exists continuously, inflammation inappropriately alters metabolic pathways and impairs insulin signaling cascades in peripheral tissues/organs such as adipose tissue, the liver and skeletal muscles, resulting in local fat deposition and insulin resistance and systemic metabolic dysregulation. In addition, inflammatory mediators, e.g., proinflammatory cytokines, and excessive nutrients, e.g., glucose and fatty acids, act together to aggravate local insulin resistance and form a vicious cycle to further disturb the local metabolic pathways and exacerbate systemic metabolic dysregulation. Owing to the critical role of nutrient metabolism in controlling the initiation and progression of inflammation and insulin resistance, nutritional approaches have been implicated as effective tools for managing obesity and obesity-associated metabolic diseases. Based on the mounting evidence generated from both basic and clinical research, nutritional approaches are commonly used for suppressing inflammation, improving insulin sensitivity, and/or decreasing fat deposition. Consequently, the combined effects are responsible for improvement of systemic insulin sensitivity and metabolic homeostasis.

scholarly journals Consequences of Vitamin A Deficiency: Immunoglobulin Dysregulation, Squamous Cell Metaplasia, Infectious Disease, and Death

2020 ◽  
Vol 21 (15) ◽  
pp. 5570
Author(s):  
Sherri L. Surman ◽  
Rhiannon R. Penkert ◽  
Robert E. Sealy ◽  
Bart G. Jones ◽  
Tony N. Marion ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Vitamin A ◽  
Squamous Cell ◽  
Sendai Virus ◽  
Vitamin A Deficiency ◽  
Renal Scarring ◽  
Critical Role ◽  
Squamous Cell Metaplasia ◽  
Pathogen Control ◽  
Tract Infections

Vitamin A is an important regulator of immune protection, but it is often overlooked in studies of infectious disease. Vitamin A binds an array of nuclear receptors (e.g., retinoic acid receptor, peroxisome proliferator-activated receptor, retinoid X receptor) and influences the barrier and immune cells responsible for pathogen control. Children and adults in developed and developing countries are often vitamin A-deficient or insufficient, characteristics associated with poor health outcomes. To gain a better understanding of the protective mechanisms influenced by vitamin A, we examined immune factors and epithelial barriers in vitamin A deficient (VAD) mice, vitamin D deficient (VDD) mice, double deficient (VAD+VDD) mice, and mice on a vitamin-replete diet (controls). Some mice received insults, including intraperitoneal injections with complete and incomplete Freund’s adjuvant (emulsified with PBS alone or with DNA + Fus-1 peptide) or intranasal inoculations with Sendai virus (SeV). Both before and after insults, the VAD and VAD+VDD mice exhibited abnormal serum immunoglobulin isotypes (e.g., elevated IgG2b levels, particularly in males) and cytokine/chemokine patterns (e.g., elevated eotaxin). Even without insult, when the VAD and VAD+VDD mice reached 3–6 months of age, they frequently exhibited opportunistic ascending bacterial urinary tract infections. There were high frequencies of nephropathy (squamous cell hyperplasia of the renal urothelium, renal scarring, and ascending pyelonephritis) and death in the VAD and VAD+VDD mice. When younger VAD mice were infected with SeV, the predominant lesion was squamous cell metaplasia of respiratory epithelium in lungs and bronchioles. Results highlight a critical role for vitamin A in the maintenance of healthy immune responses, epithelial cell integrity, and pathogen control.

scholarly journals Regulation of Inflammatory Reaction in Health and Disease

2021 ◽  
Vol 22 (10) ◽  
pp. 5277
Author(s):  
Massimo Fioranelli ◽  
Maria Grazia Roccia ◽  
Dana Flavin ◽  
Linda Cota
Keyword(s):  
Inflammatory Response ◽  
Chronic Inflammation ◽  
Inflammatory Reaction ◽  
Low Dose ◽  
Low Grade ◽  
Systems Medicine ◽  
Therapeutic Approaches ◽  
Inflammatory Conditions ◽  
Multistep Process ◽  
Health And Disease

Inflammation is a key mechanism for the clearance of infective agents and other inflammatory triggers and is pivotal for the repairing processes of the affected tissues. Inflammation is a multistep process driven by a great number of mediators which regulate specific aspects of the inflammatory response, in agreement with a well-defined chronobiological program. A great number of inflammation-related diseases show a deeply altered immune chronobiology (e.g., COVID-19-related cytokines storm). This aspect highlights the need for a deeper understanding of the inflammatory phenomenon. It is fundamental to study inflammation as a multilevel phenomenon. Of particular interest is the low-grade chronic inflammation, which is an etiological factor of many chronic diseases. Nowadays, the therapeutic approach to low grade chronic inflammation is one of the great challenges of traditional pharmacology. Currently, no drugs specifically designed for the treatment of chronic inflammatory forms are available. Today, bioregulatory systems medicine (BrSM) and low dose medicine (LDM), two pharmacological paradigms grounded in systems medicine, potentially represent new tools for the treatment of inflammation-related diseases. Scientific research has assessed the effectiveness and safety of both these therapeutic approaches, in particular for the management of chronic inflammatory conditions and chronic immunological dysregulations.

scholarly journals Pentraxin 3 deficiency protects from the metabolic inflammation associated to diet-induced obesity

2019 ◽  
Vol 115 (13) ◽  
pp. 1861-1872 ◽  
Author(s):  
Fabrizia Bonacina ◽  
Annalisa Moregola ◽  
Rémi Porte ◽  
Andrea Baragetti ◽  
Eduardo Bonavita ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Response ◽  
Immune Cell ◽  
Critical Role ◽  
Cell Phenotype ◽  
Low Grade ◽  
Pentraxin 3 ◽  
Metabolic Inflammation ◽  
Diet Induced Obesity ◽  
The Impact

Abstract Aims Low-grade chronic inflammation characterizes obesity and metabolic syndrome. Here, we aim at investigating the impact of the acute-phase protein long pentraxin 3 (PTX3) on the immune-inflammatory response occurring during diet-induced obesity. Methods and results PTX3 deficiency in mice fed a high-fat diet for 20 weeks protects from weight gain and adipose tissue deposition in visceral and subcutaneous depots. This effect is not related to changes in glucose homeostasis and lipid metabolism but is associated with an improved immune cell phenotype in the adipose tissue of Ptx3 deficient animals, which is characterized by M2-macrophages polarization and increased angiogenesis. These findings are recapitulated in humans where carriers of a PTX3 haplotype (PTX3 h2/h2 haplotype), resulting in lower PTX3 plasma levels, presented with a reduced prevalence of obesity and decreased abdominal adiposity compared with non-carriers. Conclusion Our results support a critical role for PTX3 in the onset of obesity by promoting inflammation and limiting adipose tissue vascularization and delineate PTX3 targeting as a valuable strategy for the treatment of adipose tissue-associated inflammatory response.

scholarly journals Effect of vitamin A deficiency on the immune response to epizootic diarrhoea of infant mice (EDIM) rotavirus infection in mice

1991 ◽  
Vol 65 (3) ◽  
pp. 475-485 ◽  
Author(s):  
Faruk Ahmed ◽  
David B. Jones ◽  
Alan A. Jackson
Keyword(s):  
Immune Response ◽  
Vitamin A ◽  
Antibody Production ◽  
Vitamin A Deficiency ◽  
Control Diet ◽  
Serum Antibody ◽  
Cell Mediated Immunity ◽  
Deficient Diet ◽  
Antibody Levels ◽  
Deficient Group

The effect of vitamin A deficiency on the immune response to epizootic diarrhoea of infant mice (EDIM) rotavirus was studied in mice. The virus was given by oral dosing or by intraperitoneal injection. For oral challenge, weanling mice were fed on either a control or vitamin A-deficient diet ad lib. or pair-fed the control diet to the intake of the vitamin A-deficient group. A fourth group was fed on the vitamin Adeficient diet ad lib. for 10 weeks and then refed the control diet for 2 weeks. On day 77, mice were each given 30 μl EDIM rotavirus orally and the animals were killed and examined 1 week later. The delayedtype hypersensitivity (DTH) response to picryl chloride was measured as an index of cell-mediated immunity. For intraperitoneal challenge, weanling mice were fed on either the control diet or the vitamin A-deficient diet ad lib. or pair-fed the control diet to the intake of the vitamin A-deficient group. On day 77, mice were each injected intraperitoneally with 30 μl EDIM rotavirus and 1 week later antibody production was measured. In both experiments the body-weight, liver and serum vitamin A levels of the vitamin A-deficient group were significantly lower than the control or pair-fed groups. Following oral dosing the serum antibody levels specific to rotavirus were statistically significantly lower in vitamin Adeficient animals than the control or pair-fed groups. Vitamin A-deficient mice also showed an impaired DTH response compared with the control and pair-fed animals. Animals refed vitamin A for a short period showed a partial restoration of the antibody response. Following intraperitoneal challenge no statistically significant changes were observed in the serum antibody levels between any of the dietary groups. It is concluded that vitamin A deficiency impaired antibody production when rotavirus was given orally. Vitamin A deficiency also impaired cell-mediated immunity.

Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chronic Inflammation ◽  
Ex Vivo ◽  
Human Subjects ◽  
Critical Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Tnf Α ◽  
Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

Quantification of Vitamin A in Fortified Rapeseed, Groundnut and Soya Oils Using a Simple Portable Device: Comparison to High Performance Liquid Chromatography

2013 ◽  
Vol 83 (2) ◽  
pp. 122-128 ◽  
Author(s):  
Cécile Renaud ◽  
Jacques Berger ◽  
Arnaud Laillou ◽  
Sylvie Avallone
Keyword(s):  
High Performance Liquid Chromatography ◽  
Liquid Chromatography ◽  
Vitamin A ◽  
High Performance ◽  
Vitamin A Deficiency ◽  
Developed Countries ◽  
Portable Device ◽  
Least Developed Countries ◽  
Control Food ◽  
Assay Precision

Vitamin A deficiency is still one of the major public health problems in least developed countries. Fortification of vegetable oils is a strategy implemented worldwide to prevent this deficiency. For a fortification program to be effective, regular monitoring is necessary to control food quality in the producing units. The reference methods for vitamin A quantification are expensive and time-consuming. A rapid method should be useful for regular assessment of vitamin A in the oil industry. A portable device was compared to high-performance liquid chromatography (HPLC) for three plant oils (rapeseed, groundnut, and soya). The device presented a good linearity from 3 to 30 mg retinol equivalents per kg (mg RE.kg- 1). Its limits of detection and quantification were 3 mg RE.kg- 1 for groundnut and rapeseed oils and 4 mg RE.kg- 1 for soya oil. The intra-assay precision ranged from 1.48 % to 3.98 %, considered satisfactory. Accuracy estimated by the root mean squares error ranged from 3.99 to 5.49 and revealed a lower precision than HPLC (0.4 to 2.25). Although it offers less precision than HPLC, the device estimates quickly the vitamin A content of the tested oils from 3 or 4 to 15 mg RE.kg- 1.

Research Recommendations for Applying Vitamin A-Labelled Isotope Dilution Techniques to Improve Human Vitamin A Nutrition

2014 ◽  
Vol 84 (Supplement 1) ◽  
pp. 52-59 ◽  
Author(s):  
Sherry A. Tanumihardjo ◽  
Anura V. Kurpad ◽  
Janet R. Hunt
Keyword(s):  
Public Health ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Human Subjects ◽  
The Body ◽  
Pool Size ◽  
Serum Retinol ◽  
Vitamin A Status ◽  
Status Assessment ◽  
Total Body

The current use of serum retinol concentrations as a measurement of subclinical vitamin A deficiency is unsatisfactory for many reasons. The best technique available for vitamin A status assessment in humans is the measurement of total body pool size. Pool size is measured by the administration of retinol labelled with stable isotopes of carbon or hydrogen that are safe for human subjects, with subsequent measurement of the dilution of the labelled retinol within the body pool. However, the isotope techniques are time-consuming, technically challenging, and relatively expensive. There is also a need to assess different types of tracers and doses, and to establish clear guidelines for the use and interpretation of this method in different populations. Field-friendly improvements are desirable to encourage the application of this technique in developing countries where the need is greatest for monitoring the risk of vitamin A deficiency, the effectiveness of public health interventions, and the potential of hypervitaminosis due to combined supplement and fortification programs. These techniques should be applied to validate other less technical methods of assessing vitamin A deficiency. Another area of public health relevance for this technique is to understand the bioconversion of β-carotene to vitamin A, and its relation to existing vitamin A status, for future dietary diversification programs.

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