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      Galactomannan Downregulates the Inflammation Responses in Human Macrophages via NF κB2/p100

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          Abstract

          We show that galactomannan, a polysaccharide consisting of a mannose backbone with galactose side groups present on the cell wall of several fungi, induces a reprogramming of the inflammatory response in human macrophages through dectin-1 receptor. The nuclear factor kappa-light-chain-enhancer of activated B cells 2 (NF κB2)/p100 was overexpressed after galactomannan challenge. Knocking down NF κB2/p100 using small interfering RNA (siRNA) indicated that NF κB2/p100 expression is a crucial factor in the progression of the galactomannan-induced refractoriness. The data presented in this study could be used as a modulator of inflammatory response in clinical situations where refractory state is required.

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          Dectin-1 is required for beta-glucan recognition and control of fungal infection.

          Philip Taylor, S Tsoni, Janet Willment … (2007)
          Beta-glucan is one of the most abundant polysaccharides in fungal pathogens, yet its importance in antifungal immunity is unclear. Here we show that deficiency of dectin-1, the myeloid receptor for beta-glucan, rendered mice susceptible to infection with Candida albicans. Dectin-1-deficient leukocytes demonstrated significantly impaired responses to fungi even in the presence of opsonins. Impaired leukocyte responses were manifested in vivo by reduced inflammatory cell recruitment after fungal infection, resulting in substantially increased fungal burdens and enhanced fungal dissemination. Our results establish a fundamental function for beta-glucan recognition by dectin-1 in antifungal immunity and demonstrate a signaling non-Toll-like pattern-recognition receptor required for the induction of protective immune responses.
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            The structure and synthesis of the fungal cell wall.

            Shaun M Bowman, Stephen Free (2006)
            The fungal cell wall is a dynamic structure that protects the cell from changes in osmotic pressure and other environmental stresses, while allowing the fungal cell to interact with its environment. The structure and biosynthesis of a fungal cell wall is unique to the fungi, and is therefore an excellent target for the development of anti-fungal drugs. The structure of the fungal cell wall and the drugs that target its biosynthesis are reviewed. Based on studies in a number of fungi, the cell wall has been shown to be primarily composed of chitin, glucans, mannans and glycoproteins. The biosynthesis of the various components of the fungal cell wall and the importance of the components in the formation of a functional cell wall, as revealed through mutational analyses, are discussed. There is strong evidence that the chitin, glucans and glycoproteins are covalently cross-linked together and that the cross-linking is a dynamic process that occurs extracellularly. (c) 2006 Wiley Periodicals, Inc.
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              Activation of the innate immune receptor Dectin-1 upon formation of a “phagocytic synapse”

              Helen S. Goodridge, Christopher Reyes, Courtney A. Becker … (2011)
              Innate immune cells must be able to distinguish between direct binding to microbes and detection of components shed from the surface of microbes located at a distance. Dectin-1 is a pattern recognition receptor expressed by myeloid phagocytes (macrophages, dendritic cells and neutrophils) that detects β-glucans in fungal cell walls and triggers direct cellular anti-microbial activity, including phagocytosis and production of reactive oxygen species 1, 2 . In contrast to inflammatory responses stimulated upon detection of soluble ligands by other pattern recognition receptors, such as Toll-like receptors (TLRs), these responses are only useful when a cell comes into direct contact with a microbe and must not be spuriously activated by soluble stimuli. In this study we show that despite its ability to bind both soluble and particulate β-glucan polymers, Dectin-1 signalling is only activated by particulate β-glucans, which cluster the receptor in synapse-like structures from which regulatory tyrosine phosphatases CD45 and CD148 are excluded (Supplementary Figure 1). The “phagocytic synapse” now provides a model mechanism by which innate immune receptors can distinguish direct microbial contact from detection of microbes at a distance, thereby initiating direct cellular anti-microbial responses only when they are required.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mediators Inflamm
                Journal ID (iso-abbrev): Mediators Inflamm
                Journal ID (publisher-id): MI
                Title: Mediators of Inflammation
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 0962-9351
                ISSN (Electronic): 1466-1861
                Publication date (Print): 2015
                Publication date (Electronic): 9 September 2015
                Volume: 2015
                Electronic Location Identifier: 942517
                Affiliations
                1Tumor Immunology Laboratory, IdiPAZ, La Paz Hospital, 28046 Madrid, Spain
                2Innate Immunity Group, IdiPAZ, La Paz Hospital, 28046 Madrid, Spain
                3EMPIREO S.L., 28004 Madrid, Spain
                4CIBER-BBN, 28029 Madrid, Spain
                5Respiratory Disease, IdiPAZ, La Paz Hospital, 28046 Madrid, Spain
                Author notes
                *Eduardo López-Collazo: elopezc@ 123456salud.madrid.org

                Academic Editor: Anshu Agrawal

                Article
                DOI: 10.1155/2015/942517
                PMC ID: 4579314
                SO-VID: 64b33163-4373-4f1c-9df9-de6fe864da4a
                Copyright © Copyright © 2015 Víctor Toledano et al.
                License:

                This is an open access article distributed under 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 : 13 May 2015
                Date revision received : 5 August 2015
                Date accepted : 9 August 2015
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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