For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
34
views
116
references
 Top references
cited by
0
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
1 collections
    0
    shares
      378
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Candida Infections: An Update on Host Immune Defenses and Anti-Fungal Drugs

      research-article

      Read this article at

      ScienceOpenPublisher
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Infections by fungal pathogens such as Candida albicans and non- albicans Candida species are becoming increasing prevalent in the human population. Such pathogens cause life-threatening diseases with high mortality, particularly in immunocompromised patients. Host defenses against fungal infections are provided by an exquisite interplay between innate and adaptive immune responses. However, effective anti-fungal agents for Candida infections are limited, and fungal drug resistance is a significant treatment challenge. In this review, we summarize the current understanding of host–fungal interactions, discuss the modes action of anti-fungal drugs, explore host defense mechanisms, and define the new challenges for treating Candida infections.

          Most cited references116

          • Record: found
          • Abstract: found
          • Article: not found

          Signalling through C-type lectin receptors: shaping immune responses

          Teunis B H Geijtenbeek, Sonja Gringhuis (2009)
          Key Points Crosstalk between pattern recognition receptors (PRRs) expressed by dendritic cells orchestrates T helper (TH) cell differentiation through the induction of specific cytokine expression profiles, tailored to invading pathogens. C-type lectin receptors (CLRs) have an important role in orchestrating the induction of signalling pathways that regulate adaptive immune responses. CLRs can control adaptive immunity at various levels by inducing signalling on their own, through crosstalk with other PRRs or by inducing carbohydrate-specific signalling pathways. DC-specific ICAM3-grabbing non-integrin (DC-SIGN) interacts with mannose-carrying pathogens including Mycobacterium tuberculosis, HIV-1, measles virus and Candida albicans to activate the serine/threonine protein kinase RAF1. RAF1 signalling leads to the acetylation of Toll-like receptor (TLR)-activated nuclear factor-κB (NF-κB) subunit p65 and affects cytokine expression, such as inducing the upregulation of interleukin-10 (IL-10). DC-associated C-type lectin 1 (dectin 1) triggering by a broad range of fungal pathogens, such as C. albicans, Aspergillus fumigatus and Pneumocystis carinii, results in protective antifungal immunity through the crosstalk of two independent signalling pathways — one through spleen tyrosine kinase (SYK) and one through RAF1 — that are essential for the expression of TH1 and TH17 cell polarizing cytokines. Crosstalk between the SYK and RAF1 pathways is both synergistic and antagonizing to fine-tune NF-κB activity: although Ser276 phosphorylation of p65 leads to enhanced transcriptional activity of p65 itself through acetylation, it also inhibits the transcriptional activity of the NF-κB subunit RELB by sequestering it in p65–RELB dimers, which are transcriptionally inactive. The diversity in CLR-mediated signalling provides some major challenges for the researches to elucidate and manipulate the signalling properties of this exciting family of receptors. However, the recent advances strongly support the use of CLR targeting vaccination strategies using dendritic cells to induce or redirect adaptive immune responses as well as improve antigen delivery.
          Article 0 comments Cited 397 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Syk- and CARD9-dependent coupling of innate immunity to the induction of T helper cells that produce interleukin 17.

            Salomé Leibundgut-Landmann, Olaf Gross, Matthew J. Robinson … (2007)
            The C-type lectin dectin-1 binds to yeast and signals through the kinase Syk and the adaptor CARD9 to induce production of interleukin 10 (IL-10) and IL-2 in dendritic cells (DCs). However, whether this pathway promotes full DC activation remains unclear. Here we show that dectin-1-Syk-CARD9 signaling induced DC maturation and the secretion of proinflammatory cytokines, including IL-6, tumor necrosis factor and IL-23, but little IL-12. Dectin-1-activated DCs 'instructed' the differentiation of CD4+ IL-17-producing effector T cells (T(H)-17 cells) in vitro, and a dectin-1 agonist acted as an adjuvant promoting the differentiation of T(H)-17 and T helper type 1 cells in vivo. Infection with Candida albicans induced CARD9-dependent T(H)-17 responses to the organism. Our data indicate that signaling through Syk and CARD9 can couple innate to adaptive immunity independently of Toll-like receptor signals and that CARD9 is required for the development of T(H)-17 responses to some pathogens.
            Article 0 comments Cited 301 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Antifungal agents: mode of action, mechanisms of resistance, and correlation of these mechanisms with bacterial resistance.

              Mahmoud A. Ghannoum, Louis Rice (1999)
              The increased use of antibacterial and antifungal agents in recent years has resulted in the development of resistance to these drugs. The significant clinical implication of resistance has led to heightened interest in the study of antimicrobial resistance from different angles. Areas addressed include mechanisms underlying this resistance, improved methods to detect resistance when it occurs, alternate options for the treatment of infections caused by resistant organisms, and strategies to prevent and control the emergence and spread of resistance. In this review, the mode of action of antifungals and their mechanisms of resistance are discussed. Additionally, an attempt is made to discuss the correlation between fungal and bacterial resistance. Antifungals can be grouped into three classes based on their site of action: azoles, which inhibit the synthesis of ergosterol (the main fungal sterol); polyenes, which interact with fungal membrane sterols physicochemically; and 5-fluorocytosine, which inhibits macromolecular synthesis. Many different types of mechanisms contribute to the development of resistance to antifungals. These mechanisms include alteration in drug target, alteration in sterol biosynthesis, reduction in the intercellular concentration of target enzyme, and overexpression of the antifungal drug target. Although the comparison between the mechanisms of resistance to antifungals and antibacterials is necessarily limited by several factors defined in the review, a correlation between the two exists. For example, modification of enzymes which serve as targets for antimicrobial action and the involvement of membrane pumps in the extrusion of drugs are well characterized in both the eukaryotic and prokaryotic cells.
              Article 0 comments Cited 278 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Ning Gao
                Changbin Chen
                Journal
                Journal ID (nlm-ta):
                Journal ID (publisher-id):
                Journal ID (pmc):
                Title: Infectious Diseases and Translational Medicine
                Abbreviated Title: Infect. Dis. Transl. Med.
                Abbreviated Title: Infect. Dis. Transl. Med.
                Publisher: International Biological and Medical Journals Publishing House Co., Limited (Room E16, 3/f, Yongda Commercial Building, No.97, Bonham Stand (Sheung Wan), HongKong )
                ISSN (Print): 2411-2917
                Publication date (Print): 10 April 2016
                Publication date (Electronic): 10 April 2016
                Volume: 2
                Issue: 1
                Pages: 30-40
                Affiliations
                From Key Laboratory of Molecular Virology and Immunology, Unit of Pathogenic Fungal Infection and Host Immunity, Institute Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
                From Key Laboratory of Molecular Virology and Immunology, Unit of Pathogenic Fungal Infection and Host Immunity, Institute Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
                Author notes
                Correspondence to: Changbin Chen, Tel: (+86)02154923055, Fax: (+86)02154923056, Email: cbchen@ 123456ips.ac.cn .
                Article
                DOI: 10.11979/idtm.201601005
                SO-VID: 514a8d40-af90-4fb3-a046-3afbfe7f2c90
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                Date received : 29 December 2015
                Date accepted : 20 January 2016
                Date:
                Page count
                Figures: 2, Tables: 1, References: 131, Pages: 11
                Categories
                Subject: Review

                ScienceOpen disciplines: Medicine,Infectious disease & Microbiology
                Keywords: Candida spp.,Candida albicans,Drug resistance,Host immune defenses
                Data availability:
                ScienceOpen disciplines: Medicine, Infectious disease & Microbiology
                Keywords: Candida spp., Candida albicans, Drug resistance, Host immune defenses

                Comments

                Comment on this article