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      Quantitative ELISA for SERPINA4/kallistatin

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          Abstract

          Background: SERPINA4/kallistatin is a multifunctional protein expressed from the liver; its concentration in blood circulation reflects the degree of liver dysfunction and may serve as a diagnostic/prognostic biomarker for chronic liver diseases (CLD). Materials & methods: Antibodies specific for SERPINA4/kallistatin were used for the development of an enzyme-linked immunosorbent assay (ELISA). For correlative studies, blood samples from patients with cirrhotic liver and healthy patients were collected from R.L. Jalappa Hospital & Research Centre, Kolar. Results: Interference of other SERPINs was ruled out using western blot analysis. Quantitative ELISA was developed using monospecific antibodies as capture antibodies. Conclusion: The accuracy of the developed ELISA was determined by inter- and intra-assay precision. Linearity was defined using a spiked sample with serial dilutions. Reduced levels of SERPINA4/kallistatin were observed in patients with CLD compared with healthy controls.

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          Uric acid is a danger signal activating NALP3 inflammasome in lung injury inflammation and fibrosis.

          Vincent Lagente, Sabine Charron, Sandra Girre … (2009)
          Lung injury leads to pulmonary inflammation and fibrosis through myeloid differentiation primary response gene 88 (MyD88) and the IL-1 receptor 1 (IL-1R1) signaling pathway. The molecular mechanisms by which lung injury triggers IL-1beta production, inflammation, and fibrosis remain poorly understood. To determine if lung injury depends on the NALP3 inflammasome and if bleomycin (BLM)-induced lung injury triggers local production of uric acid, thereby activating the NALP3 inflammasome in the lung. Inflammation upon BLM administration was evaluated in vivo in inflammasome-deficient mice. Pulmonary uric acid accumulation, inflammation, and fibrosis were analyzed in mice treated with the inhibitor of uric acid synthesis or with uricase, which degrades uric acid. Lung injury depends on the NALP3 inflammasome, which is triggered by uric acid locally produced in the lung upon BLM-induced DNA damage and degradation. Reduction of uric acid levels using the inhibitor of uric acid synthesis allopurinol or uricase leads to a decrease in BLM-induced IL-1beta production, lung inflammation, repair, and fibrosis. Local administration of exogenous uric acid crystals recapitulates lung inflammation and repair, which depend on the NALP3 inflammasome, MyD88, and IL-1R1 pathways and Toll-like receptor (TLR)2 and TLR4 for optimal inflammation but are independent of the IL-18 receptor. Uric acid released from injured cells constitutes a major endogenous danger signal that activates the NALP3 inflammasome, leading to IL-1beta production. Reducing uric acid tissue levels represents a novel therapeutic approach to control IL-1beta production and chronic inflammatory lung pathology.
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            Protein biomarker discovery and validation: the long and uncertain path to clinical utility.

            Nader Rifai, Michael Gillette, Steven A. Carr (2006)
            Better biomarkers are urgently needed to improve diagnosis, guide molecularly targeted therapy and monitor activity and therapeutic response across a wide spectrum of disease. Proteomics methods based on mass spectrometry hold special promise for the discovery of novel biomarkers that might form the foundation for new clinical blood tests, but to date their contribution to the diagnostic armamentarium has been disappointing. This is due in part to the lack of a coherent pipeline connecting marker discovery with well-established methods for validation. Advances in methods and technology now enable construction of a comprehensive biomarker pipeline from six essential process components: candidate discovery, qualification, verification, research assay optimization, biomarker validation and commercialization. Better understanding of the overall process of biomarker discovery and validation and of the challenges and strategies inherent in each phase should improve experimental study design, in turn increasing the efficiency of biomarker development and facilitating the delivery and deployment of novel clinical tests.
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              Uric acid promotes an acute inflammatory response to sterile cell death in mice.

              Fernando Ontiveros, Kenneth Rock, Isaac Chen … (2010)
              Necrosis stimulates inflammation, and this response is medically relevant because it contributes to the pathogenesis of a number of diseases. It is thought that necrosis stimulates inflammation because dying cells release proinflammatory molecules that are recognized by the immune system. However, relatively little is known about the molecular identity of these molecules and their contribution to responses in vivo. Here, we investigated the role of uric acid in the inflammatory response to necrotic cells in mice. We found that dead cells not only released intracellular stores of uric acid but also produced it in large amounts postmortem as nucleic acids were degraded. Using newly developed Tg mice that have reduced levels of uric acid either intracellularly and/or extracellularly, we found that uric acid depletion substantially reduces the cell death-induced inflammatory response. Similar results were obtained with pharmacological treatments that reduced uric acid levels either by blocking its synthesis or hydrolyzing it in the extracellular fluids. Importantly, uric acid depletion selectively inhibited the inflammatory response to dying cells but not to microbial molecules or sterile irritant particles. Collectively, our data identify uric acid as a proinflammatory molecule released from dying cells that contributes significantly to the cell death-induced inflammatory responses in vivo.
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                Author and article information

                Journal
                Journal ID (publisher-id): BTN
                Title: BioTechniques
                Publisher: Future Science Ltd (London, UK )
                ISSN (Print): 0736-6205
                ISSN (Electronic): 1940-9818
                Publication date (Electronic, pub): 16 September 2021
                Publication date (Print, pub): August 2021
                Volume: 71
                Issue: 5
                Pages: 556-565
                Affiliations
                1Department of Biochemistry, Sri Devaraj Urs Medical College, SDUAHER, Tamaka, Kolar, Karnataka, 563101, India
                2Department of Medicine, Sri Devaraj Urs Medical College, SDUAHER, Tamaka, Kolar, Karnataka, 563101, India
                3Department of Community Medicine, Sri Devaraj Urs Medical College, SDUAHER, Tamaka, Kolar, Karnataka, 563101, India
                4TATA Medical & Diagnostics Ltd, Mumbai, 400001, India
                Author notes
                [* ]Author for correspondence: Tel.: +91 888 600 6888; sumanthnk@ 123456gmail.com
                Author information
                https://orcid.org/0000-0002-3499-8599
                Article
                DOI: 10.2144/btn-2018-0194
                SO-VID: b7dca4a7-0247-409d-be8f-b5153718213a
                Copyright © © 2021 Dr Krishna Sumanth Nallagangula
                License:

                This work is licensed under the Attribution-NonCommercial-NoDerivatives 4.0 Unported License

                History
                Date received : 27 December 2018
                Date accepted : 26 August 2021
                Date: 16 September 2021
                Page count
                Pages: 10
                Categories
                Subject: Reports

                ScienceOpen disciplines: General life sciences,Cell biology,Molecular biology,Biotechnology,Genetics,Life sciences
                Keywords: precision,SERPINA4/kallistatin,monospecific (monoclonal) antibodies,linearity,accuracy,sensitivity,specificity ELISA,epitope,cross-reactivity
                Data availability:
                ScienceOpen disciplines: General life sciences, Cell biology, Molecular biology, Biotechnology, Genetics, Life sciences
                Keywords: precision, SERPINA4/kallistatin, monospecific (monoclonal) antibodies, linearity, accuracy, sensitivity, specificity ELISA, epitope, cross-reactivity

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