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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

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      About Blood Purification: 2.2 Impact Factor I 5.8 CiteScore I 0.782 Scimago Journal & Country Rank (SJR)

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      Proflie of Human β-Defensins 1,2 and Proinflammatory Cytokines (TNF-α, IL-6) in Patients with Chronic Kidney Disease

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          Abstract

          Background/Aim: Our aim was to determine whether altered human β-defensin (HBD), pro-inflammatory cytokines including interleukin (IL)-6 and tumor necrotic factor (TNF)-α could increase the risk of developing and exacerbation of chronic kidney disease (CKD), especially for patients with diabetic nephropathy (DN). Methods: Serum samples were obtained from 338 CKD patients and 88 sex, age-matched healthy controls. The concentrations of HBD-1 were assayed using an RIA kit. Serum levels of HBD-2, IL-6 and TNF-α were assayed using an ELISA kit. Results: Serum levels of HBD-1, IL-6 and TNF-α were significantly higher in CKD patients compared to healthy controls (P<0.05). HBD-1 levels were inversely related to estimated glomerular filtration rate (eGFR), which was the coefficient factor ( β = -0.357, P = 0.035) explaining the variability in HBD-1 in CKD. Diabetic nephropathy (DN) patients at stage 3-5 had significantly higher serum HBD-1 levels than non DN patients (P=0.00). Conclusion: Our data support the view that there is increased inflammation in CKD and DN. The inverse correlation between eGFR and serum HBD-1 which we observed is suggestive of a relationship between innate immunity and renal function and should be further investigated.

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          Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes.

          John C. Pickup (2004)
          There is increasing evidence that an ongoing cytokine-induced acute-phase response (sometimes called low-grade inflammation, but part of a widespread activation of the innate immune system) is closely involved in the pathogenesis of type 2 diabetes and associated complications such as dyslipidemia and atherosclerosis. Elevated circulating inflammatory markers such as C-reactive protein and interleukin-6 predict the development of type 2 diabetes, and several drugs with anti-inflammatory properties lower both acute-phase reactants and glycemia (aspirin and thiazolidinediones) and possibly decrease the risk of developing type 2 diabetes (statins). Among the risk factors for type 2 diabetes, which are also known to be associated with activated innate immunity, are age, inactivity, certain dietary components, smoking, psychological stress, and low birth weight. Activated immunity may be the common antecedent of both type 2 diabetes and atherosclerosis, which probably develop in parallel. Other features of type 2 diabetes, such as fatigue, sleep disturbance, and depression, are likely to be at least partly due to hypercytokinemia and activated innate immunity. Further research is needed to confirm and clarify the role of innate immunity in type 2 diabetes, particularly the extent to which inflammation in type 2 diabetes is a primary abnormality or partly secondary to hyperglycemia, obesity, atherosclerosis, or other common features of the disease.
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            Human beta-defensins.

            Lee-Jane Lu, M Pazgier, Kuender D. Yang … (2006)
            The last decade led to the discovery and characterization of several human beta-defensins. Analysis of genomic information indicates that the number of beta-defensin-like molecules encoded by the human genome may number in the tens. Growing interest in beta-defensins steadily enhances our knowledge about various aspects of their gene location, expression patterns and the transcription factors involved in their regulation in vivo. The hallmark property of beta-defensins, their antimicrobial activity, is clearly only the tip of the iceberg in the extensive network of inter-relations within the immune system in which these peptides function. Structural studies of beta-defensins provide the molecular basis for a better understanding of their properties, functions and their potential for practical applications. In this review, we present some recent advances in the studies of human beta-defensins, with an emphasis on possible correlations between their structural and functional properties.
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              Human beta-defensin-1: an antimicrobial peptide of urogenital tissues.

              E Valore, T Ganz, A Quayle … (1998)
              Antimicrobial peptides are widely distributed mediators of innate host defense in animals and plants. A 36 amino acid antimicrobial peptide belonging to the defensin family, and named human beta-defensin-1 (HBD-1), was purified recently from hemodialysate fluid, but its tissue sources were not identified. By Northern blotting, we found the highest concentrations of HBD-1 mRNA in the kidney and the female reproductive tract. In situ hybridization localized the HBD-1 mRNA in the epithelial layers of the loops of Henle, distal tubules, and the collecting ducts of the kidney and the epithelial layers of the vagina, ectocervix, endocervix, uterus, and fallopian tubes in the female reproductive tract. Using a novel technique designed to detect cationic peptides in urine, we recovered several forms of HBD-1 ranging in length from 36 to 47 amino acid (aa) residues and differing from each other by amino terminal truncation. The total concentration of HBD-1 forms in voided urine was estimated at 10-100 microg/liter, with individual variations in the total amount of HBD-1 peptides and the relative proportion of HBD-1 forms. Multiple forms of HBD-1 (size 36-47 aa) were also found in the blood plasma, bound to carrier macromolecules that released the peptide under acid conditions, and in vaginal mucosal secretions (39, 40, and 44 aa). By immunostaining, HBD-1 was located in the kidney within the lumen of the loops of Henle, but no intracellular storage sites were identified in renal or female reproductive tissues. Recombinant HBD-1 forms (36, 39, and 42 aa) and natural HBD-1 forms were antimicrobial to laboratory and clinical strains of Escherichia coli at micromolar concentrations. HBD-1 activity was not changed appreciably by low pH, but was inhibited by high salt conditions. Some of the HBD-1 peptides retained their activity against E. coli in unconcentrated (low conductance) urine, and the 36 aa form was microbicidal even in normal (high conductance) urine. Production of HBD-1 in the urogenital tract could contribute to local antimicrobial defense.
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                Author and article information

                Journal
                Journal ID (publisher-id): KBR
                Journal ID (nlm-ta): Kidney Blood Press Res
                Journal ID (doi): 10.1159/issn.1420-4096
                Title: Kidney and Blood Pressure Research
                Publisher: S. Karger AG
                ISSN (Print): 1420-4096
                ISSN (Electronic): 1423-0143
                Publication date Subscription-year: 2013
                Publication date (Print): December 2013
                Publication date (Electronic): 08 December 2013
                Volume: 37
                Issue: 6
                Pages: 602-610
                Affiliations
                aNephrology Department, Myoung-Ji Hospital; bLaboratory Medicine Department, Chung-Ang University College of Medicine, Seoul; cInformation &amp; Telecomm. Department, University of Incheon, Incheon, Korea
                Author notes
                *Hye Ryoun Kim, MD, Department of Laboratory Medicine, Chung-Ang University College of Medicine,, 224-1, Heukseok-Dong, Dongjak-Ku, Seoul 156-755 (South Korea), Tel. +82-2-6299-2718, Fax +82-2-6298-8630, E-Mail hyekim@cau.ac.kr
                Article
                Publisher ID: 355740 Other ID: Kidney Blood Press Res 2013;37:602-610
                DOI: 10.1159/000355740
                PubMed ID: 24356550
                SO-VID: 0f2643e0-14b4-4547-9ec6-30ecba20ed5d
                Copyright © © 2014 S. Karger AG, Basel
                License:

                Open Access License: This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) ( http://www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date accepted : 21 November 2013
                Page count
                Pages: 9
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Human β defensins,Innate immunity,Diabetic nephropathy,Chronic kidney disease,Pro-inflammatory cytokines
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Human β defensins, Innate immunity, Diabetic nephropathy, Chronic kidney disease, Pro-inflammatory cytokines

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