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      • Record: found
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      Metal ions in macrophage antimicrobial pathways: emerging roles for zinc and copper

      review-article
      Author(s): * , † , † , ‡ , * , † , † , ‡ , * , † , * , † , † , ‡ , 2
      Publication date (Electronic):
      Journal: Bioscience Reports
      Publisher: Portland Press Ltd.
      Keywords: copper transporter (CTR), host defence, innate immunity, monocyte, Toll-like receptor, zinc transporter, CP, ceruloplasmin, CTR, copper transporter, DC, dendritic cells, FPN1, ferroportin 1, GPI, glycosylphosphatidylinositol, IFNγ, interferon γ, IKKβ, IκB (inhibitor of nuclear factor κB) kinase β, IL, interleukin, LPS, lipopolysaccharide, MAPK, mitogen-activated protein kinase, MMP, matrix metalloproteinase, MT, metallothionein, NF-κB, nuclear factor κB, Nrf2, nuclear factor-erythroid 2-related factor 2, PDE, phosphodiesterase, ROS, reactive oxygen species, SOD, superoxide dismutase, TLR, Toll-like receptor, TNF, tumour necrosis factor, TRIF, TIR (Toll/interleukin-1 receptor) domain-containing adaptor protein inducing interferon β

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          Abstract

          The immunomodulatory and antimicrobial properties of zinc and copper have long been appreciated. In addition, these metal ions are also essential for microbial growth and survival. This presents opportunities for the host to either harness their antimicrobial properties or limit their availability as defence strategies. Recent studies have shed some light on mechanisms by which copper and zinc regulation contribute to host defence, but there remain many unanswered questions at the cellular and molecular levels. Here we review the roles of these two metal ions in providing protection against infectious diseases in vivo, and in regulating innate immune responses. In particular, we focus on studies implicating zinc and copper in macrophage antimicrobial pathways, as well as the specific host genes encoding zinc transporters (SLC30A, SLC39A family members) and CTRs (copper transporters, ATP7 family members) that may contribute to pathogen control by these cells.

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          TLR signaling augments macrophage bactericidal activity through mitochondrial ROS

          A. West, Igor E. Brodsky, Christoph Rahner … (2011)
          Reactive oxygen species (ROS) are essential components of the innate immune response against intracellular bacteria, and it is thought that professional phagocytes generate ROS primarily via the phagosomal NADPH oxidase (Phox) machinery 1 . However, recent studies have suggested that mitochondrial ROS (mROS) also contribute to macrophage bactericidal activity, although the mechanisms linking innate immune signaling to mitochondria for mROS generation remain unclear 2-4 . Here we demonstrate that engagement of a subset of Toll-like receptors (TLR1, TLR2 and TLR4) results in the recruitment of mitochondria to macrophage phagosomes and augments mROS production. This response involves translocation of the TLR signaling adapter tumor necrosis factor receptor-associated factor 6 (TRAF6) to mitochondria where it engages evolutionarily conserved signaling intermediate in Toll pathways (ECSIT), a protein implicated in mitochondrial respiratory chain assembly 5 . Interaction with TRAF6 leads to ECSIT ubiquitination and enrichment at the mitochondrial periphery, resulting in increased mitochondrial and cellular ROS generation. ECSIT and TRAF6 depleted macrophages exhibit decreased levels of TLR-induced ROS and are significantly impaired in their ability to kill intracellular bacteria. Additionally, reducing macrophage mROS by expressing catalase in mitochondria results in defective bacterial killing, confirming the role of mROS in bactericidal activity. These results therefore reveal a novel pathway linking innate immune signaling to mitochondria, implicate mROS as important components of antibacterial responses, and further establish mitochondria as hubs for innate immune signaling.
          Article 0 comments Cited 570 times – based on 0 reviews     Review now
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            The world health report 2002 - reducing risks, promoting healthy life.

            J Guilbert (2003)
            Article 0 comments Cited 415 times – based on 0 reviews     Review now
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              Metal chelation and inhibition of bacterial growth in tissue abscesses.

              Brian D Corbin, Erin Seeley, Andrea Raab … (2008)
              Bacterial infection often results in the formation of tissue abscesses, which represent the primary site of interaction between invading bacteria and the innate immune system. We identify the host protein calprotectin as a neutrophil-dependent factor expressed inside Staphylococcus aureus abscesses. Neutrophil-derived calprotectin inhibited S. aureus growth through chelation of nutrient Mn2+ and Zn2+: an activity that results in reprogramming of the bacterial transcriptome. The abscesses of mice lacking calprotectin were enriched in metal, and staphylococcal proliferation was enhanced in these metal-rich abscesses. These results demonstrate that calprotectin is a critical factor in the innate immune response to infection and define metal chelation as a strategy for inhibiting microbial growth inside abscessed tissue.
              Article 0 comments Cited 262 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biosci Rep
                Journal ID (iso-abbrev): Biosci. Rep
                Journal ID (pmc): bsr
                Journal ID (publisher-id): BSR
                Title: Bioscience Reports
                Publisher: Portland Press Ltd.
                ISSN (Print): 0144-8463
                ISSN (Electronic): 1573-4935
                Publication date (Electronic preprint): 5 June 2013
                Publication date (Electronic): 16 July 2013
                Publication date Collection: 2013
                Volume: 33
                Issue: 4
                Electronic Location Identifier: e00049
                Affiliations
                *School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Queensland 4072, Australia
                †The Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, Queensland 4072, Australia
                ‡Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland 4072, Australia
                Author notes

                1These authors contributed equally to this work.

                2To whom correspondence should be addressed (email m.sweet@ 123456imb.uq.edu.au ).
                Article
                Publisher ID: e00049
                DOI: 10.1042/BSR20130014
                PMC ID: 3712485
                PubMed ID: 23738776
                SO-VID: 06460d3b-f842-4f9a-a4cb-9da18a2af5ab
                Copyright © © 2013 The author(s) has paid for this article to be freely available under the terms of the Creative Commons Attribution Licence (CC-BY)(http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited.
                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 work is properly cited.

                History
                Date received : 28 January 2013
                Date revision received : 4 June 2013
                Date accepted : 5 June 2013
                Page count
                Figures: 3, References: 152, Pages: 14
                Categories
                Subject: Review Article
                Subject: S3

                ScienceOpen disciplines: Life sciences
                Keywords: copper transporter (ctr),host defence,innate immunity,monocyte,toll-like receptor,zinc transporter,cp, ceruloplasmin,ctr, copper transporter,dc, dendritic cells,fpn1, ferroportin 1,gpi, glycosylphosphatidylinositol,ifnγ, interferon γ,ikkβ, iκb (inhibitor of nuclear factor κb) kinase β,il, interleukin,lps, lipopolysaccharide,mapk, mitogen-activated protein kinase,mmp, matrix metalloproteinase,mt, metallothionein,nf-κb, nuclear factor κb,nrf2, nuclear factor-erythroid 2-related factor 2,pde, phosphodiesterase,ros, reactive oxygen species,sod, superoxide dismutase,tlr, toll-like receptor,tnf, tumour necrosis factor,trif, tir (toll/interleukin-1 receptor) domain-containing adaptor protein inducing interferon β
                Data availability:
                ScienceOpen disciplines: Life sciences
                Keywords: copper transporter (ctr), host defence, innate immunity, monocyte, toll-like receptor, zinc transporter, cp, ceruloplasmin, ctr, copper transporter, dc, dendritic cells, fpn1, ferroportin 1, gpi, glycosylphosphatidylinositol, ifnγ, interferon γ, ikkβ, iκb (inhibitor of nuclear factor κb) kinase β, il, interleukin, lps, lipopolysaccharide, mapk, mitogen-activated protein kinase, mmp, matrix metalloproteinase, mt, metallothionein, nf-κb, nuclear factor κb, nrf2, nuclear factor-erythroid 2-related factor 2, pde, phosphodiesterase, ros, reactive oxygen species, sod, superoxide dismutase, tlr, toll-like receptor, tnf, tumour necrosis factor, trif, tir (toll/interleukin-1 receptor) domain-containing adaptor protein inducing interferon β

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