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Immunity to Candida Infection: an Overview

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Immunity to Candida Infection: an Overview MOJ Immunology Immunity to Candida Infection: An Overview Abstract Mini Review Candida is found as a commensal of gastrointestinal and genital tract. However in contrast to many other commensals, Candida possesses a prominent ability to invade any tissue of a host presenting with innate or acquired immune deficiency. Volume 5 Issue 1 - 2017 Candida spp. is an opportunistic pathogen that has acquainted various virulence Department of Microbiology, Rural Medical College, Pravara traits facilitating host tissue colonization and invasion, and impairment of host Institute of Medical Sciences (Deemed University), India defenses. The immune system is a remarkably versatile defense system that protects an individual from invasion of pathogens including Candida. Host defense *Corresponding author: Sachin C Deorukhkar, Department mechanisms against candidiasis involve activation of an acute inflammatory of Microbiology, Rural Medical College, Pravara Institute of response by innate immunity, followed by specific T cell (cell mediated immunity) Medical Sciences (Deemed University), Loni, Maharashtra, India, Tel: +91-9545181908, +91-9850775564; Fax +91- Keywords:or B cell (humoral Candida immunity); Cell mediated mediated immunity; immune responses.Defence mechanism; Humoral 2422-273442; Email: immunity; Immune response Received: | Published: January 06, 2017 January 20, 2017 Abbreviations: AMI: Antibody Mediated Immunity; PMNL: invasion, and impairment of host defenses [5]. The immune Polymorphonuclear Leucocytes; CMI: Cell-Mediated Immunity; system is a remarkably versatile defense system that protects : Chronic Mucocutaneous Candidiasis; GI: Gastrointestinal; an individual from invasion of pathogens including Candida. The NK: Natural Killer; GM-CSF: Granulocyte-Macrophage Colony aim of this article is to comprehensively discuss the immune Stimulating Factor; MPC: Mononuclear Phagocytic Cells; PRPs: mechanisms involved in protection of host against Candida Pattern Recognition Receptors; VVC: Vulvovaginal Candidiasis; infection. TLRs: Toll-Like Receptors; CLRs: C-Type Lectin Receptors; RVVC: Recurrent Vulvovaginal Candidiasis Immunity to Candida infection The establishment of Candida infection in a susceptible host Introduction requires a series of well coordinated events to circumvent host’s Infectious diseases have always been a feature of human life and immunity. Host defense mechanisms against candidiasis involve across the globe. Until the 19th century majority of infectious diseasescontinue wereto be aattributed significant to problem bacterial, for parasitic health care and professionals viral origins activation of an acute inflammatory response by innate immunity, whereas role of fungi in human infections was less frequently followed by specific T cell (cell mediated immunity) or B cell (humoralAlthough immunity) all arms mediated of host’s immune responsessystem are [6]. implicated in recognized or documented. However the last three decades have the control of candidiasis, predominance of type of immunity is highly dependent on the site and type of infection [7]. fungal pathogens [1]. witnessed a significant rise in the incidence of infections due to Among various opportunistic fungal infections, candidiasis and macrophages play a crucial role in protection against invasive has the greatest impact due to its frequency and the severity CandidaInnate infectionsimmunity whereas;by polymorphonuclear predominance leucocytes of cell-mediated (PMNL) of complications associated with it. Candidiasis is the most opportunistic mycotic infection worldwide. Candida is found as a commensal of gastrointestinal and genital tract. However largelyimmunity controversial (CMI) is noted [7]. in control of mucosal infections [7]. The in contrast to many other commensals, Candida possesses a role of antibody mediated immunity (AMI) in candidiasis remains prominent ability to invade any tissue of a host presenting with Outcome of interaction between host’s immune system and Candida spp. may either result in the elimination of infecting pathogen from the immunocompetent host, or development innateCandida or acquired spp. isimmune the only deficiency mycotic [2]. pathogen capable of of persistent infection like chronic mucocutaneous candidiasis causing broad spectrum of clinical manifestations ranging from Candida infections mucocutaneous overgrowth to disseminated infections [3]. Although Candida can initiate infection in both immunocompetent (CMC), candidemia and/or persistent systemic and immunocompromised host, the incidence of candidiasis is inInnate immunosuppressed immunity host [6]. usually high in immunocompromised individuals. Therefore, Physical and anatomic barriers that restrict the entry of candidiasis can be rightly called as ‘disease of diseased’ [4]. Candida spp. is an opportunistic pathogen that has acquainted of defence against infection. The skin and the surface of mucus various virulence traits facilitating host tissue colonization and membranespathogens inside are included the host intissue this arecategory. considered Normal as host’sskin produces first line Submit Manuscript | http://medcraveonline.com MOJ Immunol 2017, 5(1): 00144 Copyright: Immunity to Candida Infection: An Overview ©2017 Deorukhkar 2/4 multiple substances like free fatty acids that prevent growth and multiplication of Candida spp [8]. role in opsonization, phagocytosis and other complement phagocytosis of yeast cells [8]. MBL cascade plays an importantC. Variety of cytokines and chemokines inhibitory to Candida spp albicans [8]. are secreted by epithelial cells [7]. Progessive shedding of surface functions. Both C3b and C3d fragments are capable of binding The interaction between activated C3b and the complement cells can phagocytose Candida cells [7]. receptor CR3 facilitates phagocytosis of Candida cells. C5 also epithelial cells prevents the adhesion of yeast cells. Endothelial play an important role in immunity against Candida infections. Various mechanisms control the proliferation of Candida Activation of C5 triggers the formation of C5b, which facilitates the phagocytosis and release of terminal complement components Candida surface proteins like Gpm1, Pra 1 and andspp. compositionwithin gastrointestinal of saliva prevents (GI) tract. Or opharyngealSalivary flow candidiasis prevents inthe healthy adherence individuals of yeasts by to maintainingthe mucosal a surfaces dynamic [9]. equilibrium The flow complement[14]. Binding leadsof to poor host resistance against candidiasis. between Candida ActivationGpd2 prevents of complement recognition also and regulates phagocytosis series [15].of signaling Deficiency events of during disseminated infections [14]. spp and other commensal flora [10]. contribute to innate immunity against spp. These include Candida PMNL are considered to be the most important host defence A variety of non-specific antimicrobial factors present in saliva mechanism against invasive candidiasis [7]. This is evidenced by the high incidence of systemic infections like candidemia lysozyme, lactoperoxidase histatins, calprotectin and lactoferrin Candida in patients with prolonged neutropenia or neutrophil disorders [10].Lactoferrin acts as a chelating agent that competes with oral microorganisms for free ion radicals, which are essential for bacterial and fungal multiplication. In addition, it also damages transition of Candida the fungal cell wall and activates intracellular autolytic enzymes This[16]. typeNeutrophils of leucocyte are thealso onlycontrols immunocyte the elimination that prevent of Candida the spp. from yeast to filamentous form [14]. pattern recognition receptors as well as receptors for opsonizing [10].Histatin proteins demonstrate broad spectrum antifungal antibodiesspp. from theand blood complement stream. PMNL components. additionally Among express various activity against pathogenic fungi like Candida spp, Cryptococcus mechanisms responsible for PMN mediated killing of Candida neoformans and Aspergillus fumigatus reported anti candidal activity of histatin 5. Histatin 5 when internalized by Candida leads to several [10]. deleterious Edgerton effects et al. [11]like spp., the ‘oxidative burst’ appears to be the most prominent. Oxidative burst is the process of rapid formation of reactive oxygen intermediates [14,15]. This process requires assembly damage of mitochondria and cytoplasmic membrane, efflux of Calprotectin is heterodimeric calcium and zinc binding protein of the NADPH oxidase enzyme complex in the cytoplasmic or ATP and other nucleotides and cell death [11,12]. phagosomal membrane to release superoxide [14,15]. produced by PMNL, monocytes, macrophages and mucosal host defence mechanism against candidiasis. The candidacidal keratinocytes. It ceases the Candida growth by depriving the activityNatural of NKkiller cells (NK) is largely cell system due to is production another important of granulocyte- innate demonstrated in vitro inhibitory action of calprotectin on growth produce factors responsible for activation of mononuclear offungus Candida of zinc [10]. Investigation of Steinbakk et al. (1990) macrophage colony stimulating factor (GM-CSF). NK cells also Candida C. albicans. spp [10]. phagocytic cells (MPC) and PMNL. These immune cells have only proliferation by various mechanisms like competition for The ability of PMNL and MPC to phagocytose the Candida cell, Commensal bacterial flora of GI tract inhibit marginal cytotoxic effect on nutritional and ecological niche or site of adherence, unfavourable
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