Cytokines and T Helper Cells in Diabetic Nephropathy Pathogenesis

Araújo, Liliane Silvano; Silva, Marcos Vinícius da; Silva, Crislaine Aparecida da; Monteiro, Maria Luiza Reis; Pereira, Lívia Helena de Morais; Rocha, Laura Penna; Corrêa, Rosana Rosa Miranda; Reis, Marlene Antônia dos; Machado, Juliana Reis

doi:10.4236/jdm.2016.64025

Cited by 8 publications

(5 citation statements)

References 105 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been shown that concentrations of pro-inflammatory cytokines, as IL-1, IL-6, IL-18, IL-33, IFN-γ and TNF-α actively participate in the development and progression of DN, and thus it seems that they are involved in pathogenesis, which is similar to MS. In addition, changes in the acquired immune response, especially the presence of the pro-inflammatory and effector nature of the cellular immune response profiles, in particular Th1 and Th17, as the imbalance between the interaction of cytokines and T regulatory cells, initiate the onset and progression of DN (Araujo et al, 2016), which is similar to MS. Patients with DN had a more evident Th1 profile characterized by increased IFN-γ, IL-2 and IL-12 and decreased Th2 cytokines IL-33 and IL-13, indicating that DN can be characterized by an increase in Th1 associated with suppression of Th2 response (Anand et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Association of Delta-6-Desaturase Expression with Aggressiveness of Cancer, Diabetes Mellitus, and Multiple Sclerosis: A Narrative Review

Arshad¹,

Rezapour-Firouzi

Ebrahimifar

et al. 2019

Asian Pac J Cancer Prev

View full text Add to dashboard Cite

Background:The phosphatidylinositol 3-kinase/ protein kinase B /mammalian target of rapamycin (PI3K/Akt/ mTOR) signaling regulates multiple cellular processes and organizes cell proliferation, survival, and differentiation with the available nutrients, in particular, fatty acids. Polyunsaturated fatty acids (PUFAs) are cytotoxic to cancer cells and play a critical role in the treatment of multiple sclerosis (MS) and diabetes mellitus (DM). PUFAs are produced in the body by desaturases and elongases from dietary essential fatty acids (EFAs), primarily involving delta-6-desaturase (D6D). D6D is a rate-limiting enzyme for maintaining many aspects of lipid homeostasis and normal health. D6D is important to recognize the mechanisms that regulate the expression of this enzyme in humans. A lower level of D6D was seen in breast tumors compared to normal tissues. Interestingly, the elevated serum level of D6D was seen in MS and DM, which explains the critical role of D6D in inflammatory diseases. Methods: We searched databases of PubMed, Web of Science (WOS), Google Scholar, Scopus and related studies by predefined eligibility criteria. We assessed their quality and extracted data. Results: Regarding the mTOR signaling pathway, there is remarkable contributions of many inflammatory diseases to attention to common metabolic pathways are depicted. Of course, we need to have the insights into each disorder and their pathological process. The first step in balancing the intake of EFAs is to prevent the disruption of metabolism and expression of the D6D enzyme. Conclusions: The ω6 and ω3 pathways are two major pathways in the biosynthesis of PUFAs. In both of these, D6D is a vital bifunctional enzyme desaturating linoleic acid or alpha-linolenic acid. Therefore, if ω6 and ω3 EFAs are given together in a ratio of 2: 1, the D6D expression will be down-regulated and normalized.

show abstract

Section: Discussionmentioning

confidence: 99%

Association of Delta-6-Desaturase Expression with Aggressiveness of Cancer, Diabetes Mellitus, and Multiple Sclerosis: A Narrative Review

Arshad¹,

Rezapour-Firouzi

Ebrahimifar

et al. 2019

Asian Pac J Cancer Prev

View full text Add to dashboard Cite

show abstract

“…Immune and inflammatory mechanisms play important role in the development and progression of DN, which is considered a chronic inflammatory disease [ 3 , 4 ]. Several cells, such as monocytes, macrophages, and lymphocytes, as well as chemokines and cytokines, have been implicated in this process [ 5 , 6 ]. Among them, it is known that IL-1β, IL-6, TNF-α (tumor necrosis factor-α), IL-8, MIP-1α (macrophage inflammatory protein-1α) are relevant for the development of DN, as they are potentially involved in the onset of disease complications [ 7 – 9 ].…”

Section: Introductionmentioning

confidence: 99%

Renal expression of cytokines and chemokines in diabetic nephropathy

et al. 2020

Self Cite

View full text Add to dashboard Cite

Background: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease worldwide. Inflammatory mediators have been implicated in the pathogenesis of DN, thus considered an inflammatory disease. However, further studies are required to assess the renal damage caused by the action of these molecules. Therefore, the objective of this study was to analyze the expression of cytokines and chemokines in renal biopsies from patients with DN and to correlate it with interstitial inflammation and decreased renal function. Methods: Forty-four native renal biopsies from patients with DN and 23 control cases were selected. In situ expression of eotaxin, MIP-1α (macrophage inflammatory protein-1α), IL-8 (interleukin-8), IL-4, IL-10, TNF-α (tumor necrosis factor-α), TNFR1 (tumor necrosis factor receptor-1), IL-1β, and IL-6 were evaluated by immunohistochemistry. Results: The DN group showed a significant increase in IL-6 (p < 0.0001), IL-1β (p < 0.0001), IL-4 (p < 0.0001) and eotaxin (p = 0.0012) expression, and a decrease in TNFR1 (p = 0.0107) and IL-8 (p = 0.0262) expression compared to the control group. However, there were no significant differences in IL-10 (p = 0.4951), TNF-α (p = 0.7534), and MIP-1α (p = 0.3816) expression among groups. Regarding interstitial inflammation, there was a significant increase in IL-6 in scores 0 and 1 compared to score 2 (p = 0.0035), in IL-10 in score 2 compared to score 0 (p = 0.0479), and in eotaxin in score 2 compared to scores 0 and 1 (p < 0.0001), whereas IL-8 (p = 0.0513) and MIP-1α (p = 0.1801) showed no significant differences. There was a tendency for negative correlation between eotaxin and estimated glomerular filtration rate (eGFR) (p = 0.0566). Conclusions: Our results indicated an increased in situ production of cytokines and chemokines in DN, including IL-6, IL-1β, IL-4, and eotaxin. It was observed that, possibly, eotaxin may have an important role in the progression of interstitial inflammation in DN and in eGFR decrease of these patients.

show abstract

“…Hyperglycemia in T2DM is strongly associated with the development of macrovascular and microvascular complications, which may result in decreased renal function. [3] Studies suggest that low-grade inflammation, characterized by the production of cytokines, chemokines, and adipokines, is involved in the pathogenic processes that cause T2DM and its complications [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Analysis of serum inflammatory mediators in type 2 diabetic patients and their influence on renal function

Araújo

Silva

et al. 2020

PLoS ONE

Self Cite

View full text Add to dashboard Cite

To evaluate the serum concentrations of inflammatory mediators in patients with type 2 diabetes mellitus (T2DM) with or without renal alteration (RA) function. MethodsSerum samples from 76 patients with T2DM and 24 healthy individuals were selected. Patients with T2DM were divided into two groups according to eGFR (> or < 60mL/min/ 1.73m 2 ). Cytokines, chemokines and adipokines levels were evaluated using the Multiplex immunoassay and ELISA. ResultsTNFR1 and leptin were higher in the T2DM group with RA than in the T2DM group without RA and control group. All patients with T2DM showed increased resistin, IL-8, and MIP-1α compared to the control group. Adiponectin were higher and IL-4 decreased in the T2DM group with RA compared to the control group. eGFR positively correlated with IL-4 and negatively with TNFR1, TNFR2, and leptin in patients with T2DM. In the T2DM group with RA, eGFR was negatively correlated with TNFR1 and resistin. TNFR1 was positively correlated with resistin and leptin, as well as resistin with IL-8 and leptin. ConclusionIncreased levels of TNFR1, adipokines, chemokines and decrease of IL-4 play important role in the inflammatory process developed in T2DM and decreased renal function. We also suggest that TNFR1 is a strong predictor of renal dysfunction in patients with T2DM.

show abstract

Cytokines and T Helper Cells in Diabetic Nephropathy Pathogenesis

Cited by 8 publications

References 105 publications

Association of Delta-6-Desaturase Expression with Aggressiveness of Cancer, Diabetes Mellitus, and Multiple Sclerosis: A Narrative Review

Association of Delta-6-Desaturase Expression with Aggressiveness of Cancer, Diabetes Mellitus, and Multiple Sclerosis: A Narrative Review

Renal expression of cytokines and chemokines in diabetic nephropathy

Analysis of serum inflammatory mediators in type 2 diabetic patients and their influence on renal function

Contact Info

Product

Resources

About