Chlamydia Pneumoniae Pathogen - Term Paper Example

Chlamydia pneumoniae of Chlamydia pneumoniae pathogen Chlamydia pneumoniae is apathogen under the species of Chlamydia. They comprise of chlamydia pecorum, chlamydia trachomatis and Chlamydophila psittaci. Chlamydiae species are intracellular bacteria that affect a wide variety of host mainly mammals and birds. Chlamydia pneumoniae infects humans but belonging to the chlamydia species, it has similar morphology and common development cycle. It thus possesses enzymatic systems required for DNA, RNA and protein synthesis, but uses the host cell precursors for instance nucleotides, amino acids, vitamins and other cofactors (Murphy, 2011). Chlamydia pneumoniae’s is structured in two types the infectious, non replicating elementary body (EB) and the noninfectious actively replicating reticulate body (RB). The EB and RB alternates in the development of the infectious cycle. EBs are different morphologically to the RBs as they represent different adaptations to extracellular environment and to the intracellular one correspondingly. The particle that has been infected is steady in the extracellular environment is the EB it enters the host cell, multiply and disseminate in the host extracellular environment. The pathogen completes the developmental cycle by alternating its form morphology and function. The above picture shows the cell wall of chlamydia (MOMP) major out membrane protein, (CRP) cysteine-rich protein (Murphy, 2011). The outer membrane of Chlamydia pneumoniae comprises of lipopolysaccharides (LPS) and heat-shock proteins (HSP). The LPS is composed of KDO (2-keto-3-deoxyoctonate) units with the linear trisaccharide a-KDO-(2-8)-a-KDO-(2-4)-a-Kdo. The MOMP are detectable by monoclonal antibodies, thus under these conditions that are persistence-inducing, the chlamydia Hsp60 look as if it is extremely upregulated. Chlamydia Hsp60 has proinflammatory effects by the mononuclear leukocytes being directly activated that are used for intervening the inflammatory response. The persistence of the pathogen is categorized by morphologically aberrant RBs that do not undergo cytokinesis thus form a third chlamydial type called noninfectious, nonreplicating persistence body (PB). Upon the removal of the stress factor from the body’s immune system, then PB re-enters the productive life cycle (Murphy, 2011). The EB adhering to the target cell membrane initiates penetration as it is dense and not big. It also has a firm cell wall that the SS bonds give and two other major outer membrane proteins known as the CRPs. Environmental factors that favor survival in the extracellular environment after cell lysis and switching from one cell or one host to another make EB to be resistant. The EB does not divide and is metabolically slow and is seen to have high attraction for these epithelial cells. Under this state, the main role of EB is to spread the infection from one cell to another. The presence of heparin-sulphate (proteoglycan) in the EB ensures that chlamydia pneumoniae remains in intracellular vacuole with nonacid pH and avoids the fusion of phagocytic vesicle with the lysosomes (Murphy, 2011). The EB undergoes morphological changes and restructuring in the RB that is active metabolically, bigger and divides repeatedly by binary fission. There are four times more RNA than DNA in the RB, whereas EB has an equal amount of RNA and DNA. The constant infections and divides of more cells makes the human, vulnerable to respiratory diseases. Chlamydia pneunomiae ability to infect humans and its ability to evade the immune system leads to asthma, pneumonia and different respiratory diseases that are curable in the early stages, but incurable under the chronic stages as they destroy the immune system in ways described later in this essay. Figure of chlamydia pneumoniae life cycle Expected immune response for chlamydia pneumoniae Chlamydia pneumoniae causes several diseases that are transmittable. It is the work of the immune system to make sure that it fights back the pathogen using a mechanism that is not the same from the other. There are two different ways the immune system in a human may respond to the pathogen, which are namely innate and adaptive immunities. Innate immunity is the quickest and most general response to pathogens. It is usually sufficient when dealing with a broad spectrum of invasive bacteria. The specified white blood cells (monocytes and monocyte) detect a large range of pathogens without being detected by the pathogens. They capture the pathogen and phagocytize them as the first line of anti-microbial protection. In this kind of reaction, inflammatory is necessary in the recruitment of immune cells and other relevant agents to the location of the infection. The essence that exaggerated inflammatory response can lead to undesirable effects, for instance allergic reactions. Innate immunity uses a response referred to complement that is a biochemical force, killing pathogens usually by opsonization. Innate immunity principle works properly in familiar pathogens; it will not kill or suppress Chlamydia pneumoniae since this pathogen is unfamiliar and has several evasive adaptations (Murphy, 2011). The immune system after identifying the pathogen will use adaptive immunity, which is not fast, however, dedicated in responding to unacquainted pathogens. Adaptive immunity consists of three stages. Using dendritic cell is the first stage. These dendritic cells (DCs) are specialized phagocytes with antigen presenting properties and high power of recognition of non-generic patterns and capture the pathogen. The second stage involves the DCs travel to the lymph nodes where the antigen is presented to T and B naïve cells. The third and final stage involves T and B cells mature in specialized cells against the pathogen, the mature and specialized cells travel to the infected tissue to better cope with the pathogen invasion (Murphy, 2011). Cytotoxic T cells are responsible for killing the pathogen whereas effector B cells may secrete antibodies that prevent the access of the pathogen to the host cells via humoral immunity. The essence that chlamydia pneumoniae has evasive adaptation it is hard for human immune system to suppress or kill it thus the aim of this essay to identify the evasive adaptation of this pathogen to help us develop a drug that will enable the immune system to suppress or kill the pathogen (Murphy, 2011). Adaptations of chlamydia pneumoniae that allows it to evade three defense mechanisms of the immune system Chlamydia pneumoniae is transmitted from person to person through the respiratory path. Moreover, the trachea has perfunctory barriers and innate immune mechanisms that pathogen has to evade in order to get into the host’s cells (Murphy, 2011). The inhaled pathogen has to evade the barriers of epithelial cells lining the trachea and the nasopharynx since infected airway will trigger a preliminary cascade of pro- and anti-inflammatory immune reactions (secretion of IL-8, and expression of the epithelial adhesion molecule-1) that initiate drifts and of polymophonuclear neutrophils (PMN) and acute inflammatory. The onset of antigen-specific immune response is dependent on the speed of microbial dissemination from the initial site to local lymph nodes and the destruction of intracellular bacterial is dependent on the macrophage activation that is mediated by reactive oxygen and nitrogen intermediates. Chlamydia pneumoniae uses its evasive adaptation to protect its-self against the activated macrophages by inhibiting the phagolysosomal fusion and replicating in a nonacid chlamydial inclusion (Murphy, 2011). The movement of dendritic cells (DCs) and macrophages that have being infected to regional lymph nodes initiates antigen-specific immune response. Monocytes, macrophages and DCs develop antigen-specific cell-mediated immunity by acting as antigen presenting cells (APC) secreting pro- IL-6, IL-1, IL-12 and anti-inflammatory IL-10, IL-13, cytokines which activate other immune cells. The balance of IL-12 and IL-10 that regulates the development and functional characteristics of T cells responses determine the success of the APC. MHC class 2 molecule to T CD4+ cells presents chlamydial peptides processed by APC. This leads to activation of type 1 Th cell responses that are important in regulating chlamydiae infections by inhibiting the chlamydial growth (Murphy, 2011). Chlamydia pneumoniae is structured in a way it dominates the cell-mediated responses thus escapes the immune by evading the T cell recognition by interfering with the expression of MHC molecules. The pathogen suppresses the MHC class 2 on monocytes or MHC class 1 expression on monocyte cell line. Chlamydia pneumoniae secrets a proteolytically active molecule, which degrades constitutive transcription factors USF-1 and RFX5 molecules are seen to be significant for antigen transcription during microbial infection. This leads to activation of immune purpose that is not favorable and damaging for the host as it leads to hypersensitivity and autoimmune diseases. The decreased immune system leads to lack of immune (Murphy, 2011). Hypersensitivity (HS) leads to inappropriate immune response, whereas autoimmunity creates an immune response against self-antigens thus initiating autoimmune conflict. In this stage, the chlamydia pneumoniae induces a local T cell immunosuppression and inflammatory for instance the pathogen could inhibit activated, but not nonactivated human T cell proliferation in a pathogen specific manner, heat sensitivity and multiplicity of infection dependent. This antiproliferative effect leads to T cell death associated by IL-1 Read More