Immunology of Oral Candidiasis Paper Example

Introduction

In the day to day lives, people are faced with various systematic diseases including diabetes, high blood pressure, or hypertension. Systematic diseases affect the entire body unlike other than affecting a single particular organ within the body (Ellepola, & Samaranayake, 2007). The treatment mechanisms and the occurrence of these systematic diseases predispose the patients to a wide range of fungal and bacterial infections. Upon the exposure, the bacteria and the yeast create a complex layer that tends to cover the mucosal membrane in the body. Following the increased cases of infections such as cancer and human immunodeficiency virus (HIV), there are increased cases of candidiasis infections (de Repentigny, Goupil, & Jolicoeur, 2015). Moreover, candidiasis forms significant opportunistic pathogens that affect patients in compromised groups including the patients undergoing cancer chemotherapy, persons infected with HIV, and the people undergoing a broad-spectrum antibiotic (Fidel, 2006). Oral Candidiasis commonly known as the mouth thrush is an infection that occurs when the causative agent and fungus Candida albicans mounts up in the mouth (Lilly, Leigh, McNulty, Joseph, Mercante, & Fidel, 2006).

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A pathogen is considered to be successful if it can survive effectively without being detected by the host immune defense mechanisms (Perez-Garcia, 2012). As a successful pathogen, oral candidiasis adopts strategies that aid in avoiding the detection by the host defense mechanism and finally cause other infections to the patients facing chronic illnesses. In particular, Candida albicans forms a unique parasite that can colonize, infect, and persevere on the human mucosal surfaces and thus stimulate the mucosal immune responses (de Bernardis, Sullivan, & Cassone, 2001). The fungus, Candida albicans is capable of inducing a defensive host immune response that sustains its survival in the human body. In this case, therefore, the oral health of a person is dependent on the reliability of the mucosa. The mucosa is responsible for preventing the penetration of antigenic microorganisms and macromolecules in the body (Shen, Zhang, & Lu, 2008). The mucosa is usually protected by two core independent immune systems namely; the systematic and the secretory immune systems (Guan, & Mariuzza, 2007). For instance, the oral cavity forms part of the secretory, musical immune system that can be stimulated either locally or systematically. For this reason, this makes diseases such as candidiasis to be of significant interest since both the secretory and the systematic immune systems have the potential to maintain oral health (Netea, & Marodi, 2010). Although the research of Candida has been challenging, the increasing sophistication of technology and the increasing knowledge among the scholars is creating a fruitful future in this underlying problem.

The Host Defense mechanisms against Candida albicansThe host has various defence mechanisms against the candida infection. Nevertheless, the defence depends on the rapid activation of the acute inflammatory response from the inherent immunity (Dongari-Bagtzoglou, & Fidel, 2005). The response is usually followed by an incremental stimulation that releases particular immune responses that are mediated by the T cells also known as the cellular immunity and the B cells also known as the humoral immunity. The defence mechanism occurs in a process that comprises several steps. During an infection, the initial step of inducing an immune response entails the recognition of the underlying chemical structures of the pathogens invading the body. These structures are commonly known as the pathogen-associated molecular patterns (PAMPs), and the recognition process uses the pattern recognition receptor (PRRs). The engagement between the PRR and the PAMPs is essential in necessitating the elimination of pathogens.

In eliminating the Candida infection, the host immune system begins by sensing the presence of candida fungus. The process is then followed by phagocytosis and subsequent killing of the pathogens (Fidel, 2002). Further, there is a stimulation of the cytokines which then induces the release of specific immune responses against the infection. Through this process, the phagocytosis of the Candida albicans is mediated by the combined efforts between the humoral and cellular element in the immune system therein (Tuite, Mullick, & Gros, 2004). Additionally, this process encompasses the aid of essential cells including the macrophages and neutrophils which play a significant role in necessitating the phagocytosis and the subsequent killing of Candida (Sitheeque, & Samaranayake, 2003). The cells are also critical cellular components that aid the host in generating a defence response against candida infections that are spread throughout the body. Consequently, the macrophages work in unison with the monocytes to produce the pro-inflammatory cytokines which regulate the immune response (Soysa, Samaranayake, & Ellepola, 2008). As a result, the process of killing Candida transpires through both the oxidative and the non-oxidative strategies through the help of the neutrophils and the mononuclear phagocytes.

The Relation between Candida Albicans and the Host Immune System

There is a significant interaction between Candida albicans and the host immune system. The innate primary defence mechanisms of the host are critical in mitigating the yeast colonization in the oral cavity (Ashman, Farah, Wanasaengsakul, Hu, Pang, & Clancy, 2004). In the case, the host immune system exhibits various defence mechanisms which occur in various forms including the physical barrier provided by the epithelia, the salivary factors, the secretory immunoglobulin A (SIgA), and the lingual antimicrobial peptide which is found within the mammalian epithelial tissue around the oral organs (Thein, Samaranayake, & Samaranayake, 2006). The SIgA helps in defence mechanism by aggregating and clearing the yeast and thus preventing the entry of toxic and pathogenic microorganisms to the intestinal epithelium (Steele, Leigh, Swoboda, Ozenci, & Fidel, 2001). It is also functional in the mucosal immunity as well. The flow rate of the saliva affects the process through which the clearance of the pathogenic microorganisms occurs. More importantly, the saliva has particular molecules such as the lysozyme, lactoferrin, and histatins that possess the candidacidal characteristics relevant to creating an innate immune system (Verma, Gaffen, & Swidergall, 2017).

The phagocytes within the host immune system are also active in creating a defence against an invasive candida infection. A host with normal immune response (immune-competent) has immune cells such as neutrophils, monocytes, and eosinophil that clear the candida albicans pathogens that gain access to the deeper tissues through phagocytosis. These pathogens may occur in the form of yeast and hyphal (Naglik, Moyes, Wachtler, & Hube, 2011). In the occurrence of a candida infection, the host immune system generates an acute inflammatory response to the infection where the neutrophils cells act predominantly in both numerical and in the candidacidal activity. Although these mechanisms are not always effective, the intracellular killing of the candida pathogens integrates both the oxidative and the non-oxidative techniques. In order to ensure effectiveness in killing the pathogens, it requires the augmentation of the granulocytes and macrophages by the cytokines. During the augmentation process, the forms of cytokines relevant include the interleukin-1 (IL-1), interferon-gamma (IFN-gh), and the granulocyte-macrophage-colony-stimulating factor (GM-CSF) all produced by the T-cells. The pathogenicity of the candida albican referring to the ability to cause diseases depends on the capability to which the surface molecules including the complement receptor and the mannoproteins to moderate the phagocytic responses.

The Characteristic of the Host Defense Immune against Candida AlbicansThe bone marrow produces granulocytes which are very crucial in creating a natural resistance to the candida infection. A single granulocyte ingests approximately 10 yeasts through phagocytosis (C Deorukhkar, 2017). However, it does not kill all the yeast where the proportion killed stands at 20-30% of the number of yeast ingested. During the intracellular killing process, the myeloperoxidase (MPO)-hydrogen peroxide-halide system plays a critical role. The deficiency of MPO is the primary problem in making people vulnerable to Candida albicans infection. The immunes interferon Alfa (IFN-a) and tumour necrosis factor (TNF), act independently in enhancing the candidacidal activity of the host neutrophils (Cassone, Bernardis, & Torososantucci, 2005). When the IFN-a exists in lower levels than the optimal, the TNF then acts to increase the functionality of the neutrophil effector. In this case, the cytokines such as granulocytes CSF trigger the bone marrow to produce more neutrophil and thus enhance the resistance to Candida albicans. Further, granulocytes help ion killing the mycelial aspects of candida.

Cell-mediated immunity is also crucial in fighting against candida infection (Soysa, Samaranayake, & Ellepola, 2004). Even though phagocytosis is the primary mechanisms to which the host uses in controlling candida albicans, there is a limitation on the candidacidal activity of both the granulocytes and the macrophages (Fidel, 2002). The functionality of the macrophages and the granulocytes is dependent on intensification by the cytokines which are usually induced by the T-cells. Candida infections are often found when the cell-mediated immunity is depressed. The humoral immunity is also relevant in fighting against Candida albicans (Netea, Joosten, van der Meer, Kullberg, & van de Veerdonk, 2015). It involves the serum antibodies which are significant in suppressing the growth of Candida albicans. More importantly, the saliva has sIgA which is an important immunologic factor that provides primary defence against oral candidiasis. This antibody accumulates the microorganisms and prevents the possible adherence to the mucosal epithelium (Jin, Samaranayake, Samaranayake, & Yip, 2004).

The Immunological Feature of Candidiasis

The secretory IgA and the cellular immunity play a significant role in protecting the oral mucosal surfaces from the candida albicans infection (Saunus, 2008). Undeniably, de Oliveira, Carvalho, de Gomes, Bacellar, Barros, & Carvalho, 2007), connote that there is an increased prevalence of candidiasis infections in individuals facing IgA deficiencies. Further, Dineshshankar, Sivakumar, Karthikeyan, Udayakumar, Shanmugam, & Kesavan, (2014), assert that over 50% of the patients with CMC have a reduced number of the IgA antibodies. Chronic mucocutaneous candidiasis (CMC) is a systematic disease that creates widespread lesions around the skin and the mucous membranes. CMC create a wide range of immune abnormalities including sub-optimal serum Immunoglobulin G (IgG) and Immunoglobulin M (IgM) antibodies. In the most severe types of CMC, there are cases of a defect in the transformation of lymphocytes and the stimulation of mitogen as well. Netea, Latz, Mills, & O'Neill, (2015), place patients with CMC into four independent groups named group 1 to group 4. Group one patient have a have depressed delayed hypersensitivity (DH), and they also have an abnormal macrophage migration inhibition factor (MIF). However, they have a normal lymphocyte proliferative response to Candida albicans expressed in lymphozytentransformations test (LTT) (Sharon, & Fazel, 2010). Group 2 patients lack DH but have a normal MIF and LTT. Group 3 patients have defects in all the th...