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      IL-1β/IL-6/CRP and IL-18/ferritin: Distinct Inflammatory Programs in Infections

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          Abstract

          The host inflammatory response against infections is characterized by the release of pro-inflammatory cytokines and acute-phase proteins, driving both innate and adaptive arms of the immune response. Distinct patterns of circulating cytokines and acute-phase responses have proven indispensable for guiding the diagnosis and management of infectious diseases. This review discusses the profiles of acute-phase proteins and circulating cytokines encountered in viral and bacterial infections. We also propose a model in which the inflammatory response to viral (IL-18/ferritin) and bacterial (IL-6/CRP) infections presents with specific plasma patterns of immune biomarkers.

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          Most cited references72

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          TNF-mediated inflammatory disease.

          JR Bradley (2008)
          TNF was originally described as a circulating factor that can cause necrosis of tumours, but has since been identified as a key regulator of the inflammatory response. This review describes the known signalling pathways and cell biological effects of TNF, and our understanding of the role of TNF in human disease. TNF interacts with two different receptors, designated TNFR1 and TNFR2, which are differentially expressed on cells and tissues and initiate both distinct and overlapping signal transduction pathways. These diverse signalling cascades lead to a range of cellular responses, which include cell death, survival, differentiation, proliferation and migration. Vascular endothelial cells respond to TNF by undergoing a number of pro-inflammatory changes, which increase leukocyte adhesion, transendothelial migration and vascular leak and promote thrombosis. The central role of TNF in inflammation has been demonstrated by the ability of agents that block the action of TNF to treat a range of inflammatory conditions, including rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease and psoriasis. The increased incidence of infection in patients receiving anti-TNF treatment has highlighted the physiological role of TNF in infectious diseases. 2007 Pathological Society of Great Britain and Ireland
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            Interleukin-18 regulates both Th1 and Th2 responses.

            K Nakanishi, T Yoshimoto, H Tsutsui … (2001)
            Although interleukin-18 is structurally homologous to IL-1 and its receptor belongs to the IL-1R/Toll-like receptor (TLR) superfamily, its function is quite different from that of IL-1. IL-18 is produced not only by types of immune cells but also by non-immune cells. In collaboration with IL-12, IL-18 stimulates Th1-mediated immune responses, which play a critical role in the host defense against infection with intracellular microbes through the induction of IFN-gamma. However, the overproduction of IL-12 and IL-18 induces severe inflammatory disorders, suggesting that IL-18 is a potent proinflammatory cytokine that has pathophysiological roles in several inflammatory conditions. IL-18 mRNA is expressed in a wide range of cells including Kupffer cells, macrophages, T cells, B cells, dendritic cells, osteoblasts, keratinocytes, astrocytes, and microglia. Thus, the pathophysiological role of IL-18 has been extensively tested in the organs that contain these cells. Somewhat surprisingly, IL-18 alone can stimulate Th2 cytokine production as well as allergic inflammation. Therefore, the functions of IL-18 in vivo are very heterogeneous and complicated. In principle, IL-18 enhances the IL-12-driven Th1 immune responses, but it can also stimulate Th2 immune responses in the absence of IL-12.
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              Serum ferritin is derived primarily from macrophages through a nonclassical secretory pathway.

              Matthias W Hentze, William Weiss, Daniel Morgenstern … (2010)
              The serum ferritin concentration is a clinical parameter measured widely for the differential diagnosis of anemia. Its levels increase with elevations of tissue iron stores and with inflammation, but studies on cellular sources of serum ferritin as well as its subunit composition, degree of iron loading and glycosylation have given rise to conflicting results. To gain further understanding of serum ferritin, we have used traditional and modern methodologies to characterize mouse serum ferritin. We find that both splenic macrophages and proximal tubule cells of the kidney are possible cellular sources for serum ferritin and that serum ferritin is secreted by cells rather than being the product of a cytosolic leak from damaged cells. Mouse serum ferritin is composed mostly of L-subunits, whereas it contains few H-subunits and iron content is low. L-subunits of serum ferritin are frequently truncated at the C-terminus, giving rise to a characteristic 17-kD band that has been previously observed in lysosomal ferritin. Taken together with the fact that mouse serum ferritin is not detectably glycosylated, we propose that mouse serum ferritin is secreted through the nonclassical lysosomal secretory pathway.
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                Author and article information

                Contributors
                James B. Bliska: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS Pathog
                Journal ID (iso-abbrev): PLoS Pathog
                Journal ID (publisher-id): plos
                Journal ID (pmc): plospath
                Title: PLoS Pathogens
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Print): 1553-7366
                ISSN (Electronic): 1553-7374
                Publication date (Electronic): 15 December 2016
                Publication date Collection: December 2016
                Volume: 12
                Issue: 12
                Electronic Location Identifier: e1005973
                Affiliations
                [001]Department of Internal Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, The Netherlands
                Stony Brook University, UNITED STATES
                Author notes

                The authors have declared that no competing interests exist.

                Author information
                http://orcid.org/0000-0003-3800-3138
                Article
                Publisher ID: PPATHOGENS-D-16-01178
                DOI: 10.1371/journal.ppat.1005973
                PMC ID: 5158075
                PubMed ID: 27977798
                SO-VID: f5a6f4f5-2983-48d2-9ba3-cdf51f864ba8
                Copyright © © 2016 Slaats et al
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Page count
                Figures: 2, Tables: 2, Pages: 13
                Funding
                MGN was supported by an ERC Consolidator Grant (#310372). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Review
                Subject: Biology and Life Sciences
                Subject: Biochemistry
                Subject: Proteins
                Subject: Protein Complexes
                Subject: Ferritin
                Subject: Medicine and Health Sciences
                Subject: Infectious Diseases
                Subject: Bacterial Diseases
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Diagnostic Medicine
                Subject: Signs and Symptoms
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Pathology and Laboratory Medicine
                Subject: Signs and Symptoms
                Subject: Inflammation
                Subject: Biology and Life Sciences
                Subject: Physiology
                Subject: Immune Physiology
                Subject: Cytokines
                Subject: Medicine and Health Sciences
                Subject: Physiology
                Subject: Immune Physiology
                Subject: Cytokines
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune System
                Subject: Innate Immune System
                Subject: Cytokines
                Subject: Medicine and Health Sciences
                Subject: Immunology
                Subject: Immune System
                Subject: Innate Immune System
                Subject: Cytokines
                Subject: Biology and Life Sciences
                Subject: Developmental Biology
                Subject: Molecular Development
                Subject: Cytokines
                Subject: Biology and Life Sciences
                Subject: Microbiology
                Subject: Virology
                Subject: Viral Transmission and Infection
                Subject: Medicine and Health Sciences
                Subject: Inflammatory Diseases
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Medicine and Health Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Biology and Life Sciences
                Subject: Biochemistry
                Subject: Proteins
                Subject: Acute Phase Proteins

                ScienceOpen disciplines: Infectious disease & Microbiology
                Data availability:
                ScienceOpen disciplines: Infectious disease & Microbiology

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